Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Ambulance Mistake Killed Teen After Skateboard Accident

Here is an article about the death of a kid that raises a lot of questions.

The article does not answer many of those questions.

What happened?

Melvin says Carteret General sent a respiratory therapist along in the ambulance because they decided to put a breathing tube down the child’s throat. He says Drew was not properly sedated, woke up and pulled out the tube.[1]


Not properly sedated?

Unfortunately, this does happen. Dr. Scott Weingart has a couple of podcasts where he rants about this problem.[2],[3]

Why avoid sedation?

Maybe the patient is allergic.

Use a different sedative. There are dozens available.

Maybe the patient’s blood pressure is low.

Use ketamine.

What if the patient stops breathing?

Really. This is an excuse that I have encountered with several intubated patients.

Just how stupid are some of the people who graduate from medical school?

The patient is already intubated and on a ventilator (or being ventilated by BVM [Bag Valve Mask] resuscitator).

What do we do for someone who stops breathing?

Ventilate – for example by BVM until an endotracheal tube is placed.

If an endotracheal tube has already been placed, does anyone really care if the patient stops breathing?

And . . .

. . . ketamine.

Ketamine is a sedative that usually does not depress the patient’s respiratory drive.

And there is one more minor point to consider.

Most patients are intubated with the assistance of not just sedatives, but also paralytics.

If you are breathing after receiving a paralytic, somebody did something wrong. A paralytic is supposed to stop every muscle in the body from contracting – except the heart.

It could be that there was an omission of adequate doses of more than two types of drugs – sedatives and paralytics and, as Dr. Weingart will point out, pain medicine, because sedatives do not usually provide pain relief . . .

. . . except for ketamine.

It is a versatile drug, that ketamine.

The patient woke up and pulled the tube out.

Which would make you happier?

1. I have to ventilate this patient through the tube that is already in place.

2. I have to place the tube back in the trachea during transport because you neglected to provide adequate sedation. Even if reintubated excellently, intubation has many complications.

That should be the antidote to the argument that sedation is a bad thing (what if he stops breathing?), because it should be obvious that not breathing, but being ventilated is much better than not being sedated and being so agitated that the patient removes his airway.

Just put it back in!

That is the response, except . . .

The attorney says when those in the ambulance re-inserted the tube, it went into the teen’s esophagus, rather than his trachea.[1]


That happens.

Esophageal intubation is no big deal.

Just ventilate and place the tube in the trache. If the tube cannot be properly placed, we can use the BVM for ventilation or perform a crichothyrotomy. Both are acceptable means of ventilation.

He says Drew was given sedatives, and the teen, unable to breathe on his own, went without oxygen for about 35 minutes.[1]


Not recognizing a tube that has been placed in the esophagus, or one that has migrated to the esophagus, is just plain bad patient care.

Nobody should be intubating without waveform capnography to confirm placement.

Even without waveform capnography, there should not be a problem. All intubated patients should have continual assessment, which should identify a problem long before brain death.

Again, the worst case is that the patient is ventilated by BVM or crichothyrotomy.

We do not have details about what happened, but the patient appears to have arrived at the hospital without brain function. Was that due to the original injury, with the esophageal intubation only complicating matters?

There is not enough information to tell, but when the tube is left in the esophagus, it is kind of like leaving your fingerprints all over a knife sticking out of a dead guy’s chest. People are not going to spend a lot of time looking for another cause of death.

Capnography has been recommended in ACLS (Advanced Cardiac Life Support) since 2000, if not earlier.[4]

How difficult is assessment for an improperly placed tube (all tubes should be considered improperly placed and continually reassessed)?[5]

Melvin says the ambulance crew diverted to CarolinaEast in New Bern, and the ER doctor there immediately recognized the tube was in the wrong place.[1]


We like to find evidence that confirms what we believe. (I believe that the tube is where I want it to be. I saw the tube go through the cords.)

This is dangerous.

We need to look for evidence that we are wrong.

If we are not constantly looking for evidence that we are wrong, we will make a lot more mistakes than we should.

Science is a method of looking for evidence that we are wrong. That is why science keeps improving.

We need to take a more scientific approach to patient care. . .

. . . and have I mentioned ketamine? Science shows that ketamine is safe and effective.

I have more information here – Further Details on ‘Ambulance Mistake Killed Teen After Skateboard Accident’


[1] LAWSUIT: Ambulance Mistake Killed Teen After Skateboard Accident
Updated: Wed 9:14 PM, Nov 06, 2013

[2] Intubated ED Patients are Still Not Receiving Sedation
by Scott D. Weingart, MD.
Podcast page

[3] ED patients being intubated and then not sedated or pain-controlled
by Scott D. Weingart, MD.
Podcast page

[4] You had me at ‘Controversial post for the week’ – Part I
Tue, 22 Oct 2013
Rogue Medic

[5] More Intubation Confirmation
Sun, 27 Apr 2008
Rogue Medic


Ketamine Myths Debunked in Four Podcasts


Many people are still afraid of using ketamine in EMS, because of various myths.

Dr. Minh Le Cong of PHARM – PreHospital And Retrieval Medicine has four excellent podcasts debunking the scare stories told by people unfamiliar with ketamine.

Go listen to all four podcasts about these ketamyths medical urban legends –

PHARM Podcast 75 Ketamine MythBusters Part 1 – Blowing your mind

Ketamyth 1 –

It has traditionally been avoided in the management of patients with traumatic brain injury owing to concerns that it may increase intracranial pressure.[1]


Does ketamine dangerously raise ICP (IntraCranial Pressure) for patients with head injuries?

Concerns regarding the potential for ketamine to raise ICP stem from small case control series several decades ago in patients with abnormal CSF flow dynamics [53].[1]


Medical myths are based largely on anecdote and unreasonable extrapolation, rather than evidence.

This myth assumes the effect should be generalized beyond the abnormal subset of patients in the study to all head injured patients and possibly to those in the room when ketamine is given to patients with head injuries.


Was the abnormal subset of patients in that study representative of the entire study?


Does ketamine cause increased damage to patients with head injuries?

Several recent studies have refuted the original findings and showed no statistically significant rise in ICP in brain injured patients who are sedated with ketamine [56].[1]


But we should still avoid ketamine just to be safe, right?

The antagonism of NMDA receptors decreases the release of neurotoxic glutamate and may impart a protective effect in patients with traumatic brain injury [60].[1]


But we were told by experts that ketamine is dangerous.

Therefore ketamine is indicated particularly as an induction agent in patients with TBI and haemodynamic instability. It may have a role for refractory seizure activity.[1]


But some expert once said that there is a danger, so I am afraid the lawyers will get me, because I know less about medicine than lawyers do!!!11!!!

Based on its pharmacological properties, ketamine appears to be the perfect agent for the induction of head injured patients for intubation.[2]


We become dangerous when we base our decisions on politics, rumor, and bias, rather than valid evidence.

Go listen to the podcast.

And listen to the rest of the series of ketamine myth debunking –

Ketamyth 2 –

PHARM Podcast 76 Ketamine MythBusters Part 2 – Take the pressure down

Does it cause dangerous tachycardia and hypertension? How useful is it in the haemodynamically unstable patient?[3]


Go ahead. Bet that the myth is true. You know that your inner anecdotalist wants you to.

Ketamyth 3 –

PHARM Podcast 77 Ketamine MythBusters Part 3 – Are you mad enough?

Does it cause dangerous psychosis? How useful is it in the agitated patient? How common is the so called emergence delirium? What can you do if it happens? What can you do to prevent it from happening?[4]

Live dangerously. Bet on the myths. 😉

Ketamyth 4 –

PHARM Podcast 78 Ketamine MythBusters Part 4 – A fitting end?

Ketamine and epilepsy. Does it cause seizures? can it be used to manage seizures?[5]


For non-Commonwealth readers, who may be unfamiliar with the term fitting, fitting means having a seizure.

Ketamine has advantages over traditional antiseizure medications with less respiratory depression and hypotension[5]


We can rely on anecdote-based myths, or we can look at the actual evidence and learn the truth.

The great tragedy of Science — the slaying of a beautiful hypothesis by an ugly fact. – Thomas Henry Huxley.


[1] Sedation in traumatic brain injury.
Flower O, Hellings S.
Emerg Med Int. 2012;2012:637171. doi: 10.1155/2012/637171. Epub 2012 Sep 20.
PMID: 23050154 [PubMed]

Free Full Text from PubMed Central.

[2] Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury.
Filanovsky Y, Miller P, Kao J.
CJEM. 2010 Mar;12(2):154-7. Review. No abstract available.
PMID: 20219164 [PubMed – indexed for MEDLINE]

Free Full Text from CJEM.

[3] PHARM Podcast 76 Ketamine MythBusters Part 2 – Take the pressure down
PHARM – PreHospital And Retrieval Medicine
by rfdsdoc on July 20, 2013
Podcast page with links to evidence.

[4] PHARM Podcast 77 Ketamine MythBusters Part 3 – Are you mad enough?
PHARM – PreHospital And Retrieval Medicine
by rfdsdoc on July 31, 2013
Podcast page with links to evidence.

[5] PHARM Podcast 78 Ketamine MythBusters Part 4 – A fitting end?
PHARM – PreHospital And Retrieval Medicine
by rfdsdoc on August 14, 2013
Podcast page with links to evidence.


FDA Warning of Zyprexa Deaths – NOT With the Drug used by EMS or in the Emergency Department


Today the FDA (Food and Drug Administration) sent out a safety announcement about long-acting olanzapine (Zyprexa Relprevv).

This is not the form of olanzapine (Zyprexa) used by EMS or used in the ED (Emergency Department).

Post-injection Delirium Sedation Syndrome (PDSS): Patients are at risk for severe drowsiness (including unconsciousness or coma) and/or confusion and disorientation after each injection and must stay at the doctor’s office or clinic for at least 3 hours after the injection is given. ZYPREXA RELPREVV is only prescribed by doctors who are enrolled in the ZYPREXA RELPREVV Patient Care Program to patients who are also enrolled.[1]


The affected medication is packaged as Zyprexa Relprevv, the long-acting version of olanzepine.

Image credit.[2]

We would use olanzapine in its regular formulation, which has been available as a generic since 2011, when Eli lilly’s patent expired.

The patent on Zyprexa Relprevv does not expire until September 30, 2018, so it is only available as an expensive version from Eli Lilly.[3]

What happened?

FDA is investigating two unexplained deaths in patients who received an intramuscular injection of the antipsychotic drug Zyprexa Relprevv (olanzapine pamoate). The patients died 3-4 days after receiving an appropriate dose of the drug, well after the 3-hour post-injection monitoring period required under the Zyprexa Relprevv Risk Evaluation and Mitigation Strategy (REMS). Both patients were found to have very high olanzapine blood levels after death.[4]


Why 3 hours?

Click on images to make them larger.

Post-injection delirium/sedation syndrome events and time to initial onset, incapacitation, and hospitalization. The middle line inside the box is the median 50th percentile; left border of the box is the 25th percentile and right borders of the box is the 75th percentile; left whisker is the 10th percentile and right whisker is the 90th percentile.[5]


All patients demonstrated symptoms within 5 hours of injection, so onset 3 to 4 days after injection seems unlikely. This medication can only be given in the clinic or doctor’s office, so an extra dose is improbable.

How likely is it that the cause of death is the medication?

It would seem unlikely, except that Both patients were found to have very high olanzapine blood levels after death.

The FDA will investigate this and may find out the cause(s) of death, or may nor find out the cause(s) of death, but it does not appear to be something that affects emergency patients.

These patients may present to EMS, or the ED, from a doctor’s office or clinic and we should be familiar with treatment.

Symptoms appear to be less severe than with an overdose of olanzapine, so management should be just supportive care (assess blood sugar, vital signs, level of consciousness, . . .), only treating what truly needs to be treated (seizures, airway compromise, . . .).

As discussed by McDonnell et al. [5], the probable mechanism most likely involves accidental entry of the medication into the blood stream following blood vessel injury during the injection process. The similarity in incidence of olanzapine LAI PDSS (0.07% of injections) to that of Hoigne’s syndrome following accidental intravascular injection of penicillin procaine G (0.08% of injections) [6] suggests that these findings may be approximating the naturally occurring background rate for accidental direct or indirect intravascular injection during any intramuscular injection process.[5]


Accidental intravenous, or intra-arterial, injection does not seem to be a possible cause of deaths that happen several days later.

We do not have other information on the patients, such as when they were last seen without any symptoms, what other medications they were taking, what other medical conditions were present, whether there were signs of trauma, . . . , so the only thing to do is wait for more information.

If you carry olanzapine, there is no reason not to keep using it as before.

If this encourages you to switch to ketamine, I do not see any problem with that decision.


[1] Important Safety Information about ZYPREXA® RELPREVV™ (olanzapine) For Extended Release Injectable Suspension
Eli Lilly
Home page.

[2] ZYPREXA RELPREVV (olanzapine pamoate) kit
[Eli Lilly and Company]

FDA Label

[3] Generic Zyprexa Relprevv Availability
Information page.

[4] Zyprexa Relprevv (Olanzapine Pamoate): Drug Safety Communication – FDA Investigating Two Deaths Following Injection
Posted 06/18/2013
FDA Drug Safety Communication

[5] Post-injection delirium/sedation syndrome in patients with schizophrenia treated with olanzapine long-acting injection, I: analysis of cases.
Detke HC, McDonnell DP, Brunner E, Zhao F, Sorsaburu S, Stefaniak VJ, Corya SA.
BMC Psychiatry. 2010 Jun 10;10:43. doi: 10.1186/1471-244X-10-43.
PMID: 20537128 [PubMed – indexed for MEDLINE]

Free Full Text from BMC Psychiatry.


Equipoise and Ethics and IRBs, Oh My!

In the comments to what I wrote yesterday about seizures and a study comparing lorazepam (Ativan), diazepam (Valium), and placebo,[1] Brooks Walsh had the following comment –

Although I’ve read the study before, I am only wondering now how the IRB for Alldredge 2001 thought there was “equipoise” between placebo and benzos.


Not just he race horse mentioned in one of the songs from Guys and Dolls, or a mouse being a raced in Stalag 17. Maybe I should have written this with Nathan Detroit being stranded on Gilligan’s Island, or I could try that for something on ketamine. 😉

In short, clinical equipoise means that there is genuine uncertainty in the expert medical community over whether a treatment will be beneficial.[2]

In many cases, there is equipoise, but we are too biased to realize how little we know about the treatments we are using. Epinephrine in cardiac arrest, ventilations in cardiac arrest, and prehospital use of backboards and EMS collars are a few examples of this kind of bias.

We have been using the treatments for so long that we can’t imagine that we have been doing something useless, or even worse, something harmful.

Our knowledge of the effects of the treatments we use may not be any better than what we see in the video of the the knowledge of the horses that the characters are betting on. Selective memory and wishful thinking are the basis for our choices.

The diazepam vs. lorazepam vs. placebo study is a bit of a different situation. EMS was still largely doing what medical directors felt could safely be moved from the ED (Emergency Department) to the EMS setting, but we did not know if any of it worked as used by EMS. We also worried that the respiratory depression would be common and cause more problems than the potential benefits of stopping the seizures.

The doses were small.

With the doses we used, I felt that the seizures were more likely to stop on their own, rather than because of the small doses of diazepam that I could give – up to 5 mg at a time.

A lot of people (including emergency physicians) do not seem to realize that most seizures are self-limiting. EMS is not treating aggressively for these seizures, which would go away even if treated with homeopathy (or any other placebo treatment).

We are treating all of the patients who might have status epilepticus because the outcome for those who do have status epilepticus is so bad when they are not treated aggressively.

There do not appear to have been any studies that compared EMS administered benzodiazepines with EMS not administering benzodiazepines. There are only two studies that I found published before this study was published, but both were published years after this study began.[3],[4]

Here is what the authors wrote about the state of the evidence before they began the study.

Several randomized trials of drug treatment for status epilepticus in hospitalized patients have been conducted.1,3,4 However, patients with seizures and status epilepticus are commonly encountered outside of the hospital by emergency-medical-services personnel. Traditionally, these patients have been transported quickly to emergency departments for treatment. In recent years, many emergency-medical-services systems have implemented protocols that allow the intravenous administration of benzodiazepines (principally diazepam) by paramedics. However, the risks and benefits of treatment with benzodiazepines outside of the hospital have not been studied. Potential benefits include the prevention of systemic and neurologic sequelae of prolonged convulsive seizures. Potential risks include respiratory depression and cardiovascular compromise associated with benzodiazepines and misdiagnosis leading to inappropriate treatment.2 [5]

It is easy to forget how much things have changed in a couple of decades.

This study began to enroll patients January 4, 1994, so the planning of the study began over twenty years ago.

Because of the emergency nature of status epilepticus and the unconscious state of the patient, enrollment took place under a waiver of informed consent pursuant to federal regulations. The rationale for the waiver was that diazepam, lorazepam, or no benzodiazepines were used by various emergency-medical-services systems for the management of status epilepticus at the time of the study and that insufficient data were available to determine the optimal out-of-hospital treatment for this condition.[5]

In other words, we doid not know what was best.

In another word – equipoise.

The average time from patient contact to arrival in the ED was only 15 minutes.

Click on images to make them larger.
The outcomes showed that waiting until the patient is in the ED to treat the seizure is not a good idea.

Before this study, that was just an opinion.

After the study, it had been demonstrated objectively.
Some people have similar criticism about a lot of other treatments that have never been demonstrated to improve outcomes.

A year ago yesterday, the Hagihara study[6] comparing cardiac arrest outcomes with and without epinephrine was published in JAMA.

In the editorial accompanying that paper, Dr. Clifton Callaway wrote the following about the state of equipoise of epinephrine in cardiac arrest.

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.[7]

Similarly –

The best available observational evidence indicates that epinephrine ventilation may be harmful to patients during cardiac arrest, and there are plausible biological reasons to support this observation.

or –

The best available observational evidence indicates that epinephrine use of backboards and EMS collars may be harmful to patients during cardiac arrest with unstable injuries of the spine, and there are plausible biological reasons to support this observation.

When we base our treatments on hunches, or expert opinions, we will eventually have to go back and find out if they work.

Or, as a quote attributed to John Wooden puts it –

If You Don’t Have Time to Do It Right, When Will You Have Time to Do It Over?

We expect that our experts will have gotten combinations of treatments just right on the first try, or the second try, or even on the third try, even though there is no good reason to expect this.

Experts have a history of repeated failure and eventual success, not a history of continual success.

An expert is a man who has made all the mistakes which can be made in a very narrow field. – Niels Bohr.

Image credit.
Is it safe to bet on the opinions of experts?

That depends on what they are expressing opinions on, how accurate they have been with previous opinions, and the quality of the information on which they base their opinions.

In this case, the odds are against the experts.

Maybe we think that because an expert has made all of the known mistakes in a field, the expert cannot make any more mistakes in the same field.

We continue to think that ROSC (Return Of Spontaneous Circulation) is the most important factor in resuscitation, but we have proven that to be false.

Norepinephrine and high-dose epinephrine produced more ROSC than standard-dose epinephrine.

If ROSC were the most important factor in resuscitation, we would use these treatments, rather than standard-dose epinephrine.

We do not.

Norepinephrine and high-dose epinephrine produce more brain damage than standard-dose epinephrine.[8]

We know that epinephrine produces brain damage, but we foolishly believe that the doses we use are not toxic.

We need to demonstrate the safety and efficacy of epinephrine in cardiac arrest.

We need to demonstrate the safety and efficacy of ventilations in cardiac arrest.

We need to demonstrate the safety and efficacy of backboards and EMS collars for injuries to the spine.

The stakes are too high to keep playing a hunch – whether Paul Revere, Valentine, Epitaph, epinephrine, ventilation, or backboards and EMS collars.

Look at how we rejected making high-dose epinephrine routine –

A meta-analysis and other studies have found improved ROSC, but none have demonstrated a survival benefit of high-dose epinephrine versus standard-dose epinephrine in cardiac arrest.135,268,–,272 [8]

What do we do with the same, or worse, results when the comparison is between epinephrine and not drug?

There are no RCTs that adequately compare epinephrine with placebo in treatment of and outcomes related to out-of-hospital cardiac arrest. A retrospective study267 compared epinephrine to no epinephrine for sustained VF and PEA/asystole and found improved ROSC with epinephrine but no difference in survival between the treatment groups.[8]

We have to do something.

We rejected high-dose epinephrine, which had improved ROSC, but no improved survival.

We embrace standard-dose epinephrine, which has improved ROSC, but no improved survival.

We might as well be playing the ponies.

It is reasonable to consider administering a 1 mg dose of IV/IO epinephrine every 3 to 5 minutes during adult cardiac arrest (Class IIb, LOE A).[8]


LOE is Level Of Evidence. A is the highest ranking of evidence.

That means that the AHA (American Heart Association) is confident that they have excellent evidence, but that the evidence is not enough to give anything more than their weakest recommendation for use.

This Class IIb recommendation remains unaffected, even though the studies published continue to be neutral or negative.

Epinephrine equipoise is nothing new. what is new is that it is being acknowledged.


[1] Giving New Meaning to Carpe Diem
Thu, 21 Mar 2013
Rogue Medic

[2] Clinical equipoise

[3] Pediatric emergency medicine practice patterns: a comparison of pediatric and general emergency physicians.
Schweich PJ, Smith KM, Dowd MD, Walkley EI.
Pediatr Emerg Care. 1998 Apr;14(2):89-94.
PMID: 9583386 [PubMed – indexed for MEDLINE]

[4] Prehospital management of the seizure patient.
Nicholl JS.
Emerg Med Serv. 1999 May;28(5):71-5; quiz 77.
PMID: 10537415 [PubMed – indexed for MEDLINE]

Free Full Text Download in Word format from angelfire.com.

[5] A comparison of lorazepam, diazepam, and placebo for the treatment of out-of-hospital status epilepticus.
Alldredge BK, Gelb AM, Isaacs SM, Corry MD, Allen F, Ulrich S, Gottwald MD, O’Neil N, Neuhaus JM, Segal MR, Lowenstein DH.
N Engl J Med. 2001 Aug 30;345(9):631-7. Erratum in: N Engl J Med 2001 Dec 20;345(25):1860.
PMID: 11547716 [PubMed – indexed for MEDLINE]

Free Full Text from N Engl J Med.

[6] 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.

[7] 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.

This is definitely worth listening to.

[8] Epinephrine
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.2: Management of Cardiac Arrest
Medications for Arrest Rhythms
Free Full Text from Circulation.

Alldredge BK, Gelb AM, Isaacs SM, Corry MD, Allen F, Ulrich S, Gottwald MD, O’Neil N, Neuhaus JM, Segal MR, Lowenstein DH. (2001). A Comparison of Lorazepam, Diazepam, and Placebo for the Treatment of Out-of-Hospital Status Epilepticus New England Journal of Medicine, 345 (25), 1860-1860 DOI: 10.1056/NEJM200112203452521

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

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) DOI: 10.1001/jama.2012.294


Excited Delirium – Episode One of Rogue Medic Rants podcast


Matt Fults and Brad Buck are hosting a podcast for me at Standing Orders – The Podcast.

They share a delusions that there is not enough Rogue Medic on the internet. 😕

Their solution is to give me my own podcast on their site. 😎

They mention that they are excited; I point out that they are delusional; so the first podcast is perhaps the best way to combine these into one diagnosis – Excited Delirium. 😯

Episode One: Excited Delirium


Image credit.

Does anything suggest excited delirium as succinctly as that image?

No. That is not a picture of me.

I am putting all of the links on the Rogue Medic Rants page for each post. You can listen to the podcast and look up the links all from one page.

This podcast has almost ten minutes of introduction because it is the first one. Later podcasts will have much less of an introduction, or maybe no introduction.

After the introduction, the discussion of excited delirium is less than 15 minutes long.

I apologize for not being well prepared for the podcast. I had all of my notes set for a different podcast, but we decided that one will be done at a different time for a variety of reasons. I hope that I provided enough information in the notes to correct any inaccuracies in the podcast. I think the only one was the dose of ketamine – the starting dose should be 5 mg/kg, not 2 mg/kg. 2 mg/kg is great for procedural sedation, but not for taking down a violent patient.

I will try to keep the podcasts short.

I may have some longer podcasts with a guest, or with several guests. I have already invited Peter Canning of Street Watch: Notes of a Paramedic. He is currently doing an excellent series on What BLS Should Be Doing Now.

Matt, Brad, and I will be at Gathering of Eagles, so feel free to talk to anyone with a shirt with the Standing Orders logo on it. I don’t have one, so just look for someone who looks weird. 😳

There will probably be some Standing Orders and/or Rogue Medic Rants podcasts from Gathering of Eagles. Not live, but probably without much of a delay.

One of the topics I really want to talk with the attendees about is the recent spinal immobilization research and research reviews, but that is a topic for some other posts.

Let me know what you think about the podcast. Ways to improve it – I am no Morgan Freeman, but I will try to make it easy to listen to.

Suggestions for topics and guests, further information on a podcast, and criticism – all are welcome.

Likewise, let Matt and Brad know what you think.

Rogue Medic Rants


Drug shortages leading to better EMS protocols

MIEMSS (Maryland Institute for Emergency Medical Services Systems) has posted some changes to their protocols that are in response to the drug shortages affecting EMS.

This is good news, even though two of the three drugs being used as replacements are also subject to drug shortages. That is one of the problems with the drug shortage – the replacements end up suffering from increased demand to replace the original drugs.

Some of the drugs do not need any replacement, such as IV (IntraVenous) furosemide (Lasix) for CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) patients. The best thing we can do is to stop giving the drug and to stop giving any other diuretic for a medical condition that is not effectively treated with diuretics.[1]

Pain management drugs are important and availability is important.

The continuing medication shortage continues to affect Maryland EMS Operational Programs (EMSOPs). Morphine is among the medications that EMSOPs have had difficulty restocking.

Because of the importance of successfully managing pain in out-of-hospital medicine, the Protocol Review Committee has looked into alternatives to Morphine for Maryland EMS. MIEMSS has emergently included fentanyl in the 2012 Maryland Medical Protocols effective immediately. Please see the attached protocol pages.[2]


Unfortunately, the obvious substitutes are also in short supply – fentanyl (Sublimaze), hydromorphone (Dilaudid), and other opioids.[3]

One interesting part of the Maryland protocols is the addition of abdominal pain to their standing orders for morphine or fentanyl administration. The Maryland protocols have leapfrogged past Pennsylvania’s protocols with a couple of big changes.

Image credit.

Even a surgical journal has research showing that treating undifferentiated abdominal pain with opioids does not make diagnosis more difficult.

The literature addressing early pain relief for abdominal pain is characterized by weaknesses, but there is a common theme suggesting that analgesia is safe. Pending further research, which should address some of the shortcomings of extant studies, a practice of judicious provision of analgesia appears safe, reasonable and in the best interests of patients in pain.


A much more recent Cochrane Review comes to the same conclusion.

Eight studies fulfilled the inclusion criteria. Differences with use of opioid analgesia were verified in variables: Change in the intensity of the pain, change in the patients comfort level.

The use of opioid analgesics in the therapeutic diagnosis of patients with AAP does not increase the risk of diagnosis error or the risk of error in making decisions regarding treatment.


If we were to ask the patients what they prefer, I expect that a lot would choose to decrease their pain, even if there is the minimal possibility of alteration in physical assessment. That alteration may be for the better – if the patient is not in severe pain at the slightest touch, the patient may be able to localize the pain, which is a big part of the physical assessment of undifferentiated abdominal pain.


[1] Drug Shortages Affect Those Still in the Dark Ages – Furosemide
Rogue Medic
Thu, 26 Aug 2010

[2] NEW (June 2012) – Emergency Medication Addition Due to Medication Shortage: FENTANYL
Maryland Institute for Emergency Medical Services Systems
June 12, 2012
MIEMSS page with links to this and other updates and to current protocols

There is also information at that page about the following two changes because of the drug shortage –

NEW (April 2012) – Emergency Medication Addition Due to Medication Shortage: KETAMINE

NEW (May 2012) – Emergency Medication Addition Due to Medication Shortage: DIAZEPAM

[3] Current Drug Shortages Index
Current Drug Shortages Index

[4] Effect on diagnostic efficiency of analgesia for undifferentiated abdominal pain.
Thomas SH, Silen W.
Br J Surg. 2003 Jan;90(1):5-9. Review.
PMID: 12520567 [PubMed – indexed for MEDLINE]

[5] Analgesia in patients with acute abdominal pain.
Manterola C, Vial M, Moraga J, Astudillo P.
Cochrane Database Syst Rev. 2011 Jan 19;(1):CD005660. Review.
PMID: 21249672 [PubMed – indexed for MEDLINE]


Serious adverse events during procedural sedation with ketamine – Part I


What contributes to adverse events with the use of ketamine for PSA (Procedural Sedation and Analgesia) in children?

The pre-PSA use of fentanyl or morphine or concomitant use of midazolam and/or atropine was not associated with an increased in adverse event in either IM or IV ketamine (Table 1).[1]

However, there was a trend toward different rates of adverse events with the use of some medications in addition to ketamine. A larger study would be able to tell if these trends are real or just normal statistical variation.

The use of morphine, fentanyl, and midazolam would be expected to cause some adverse effects, but midazolam seems to provide protection from adverse events.

Morphine and fentanyl were used so infrequently, that drawing any conclusions from such small numbers is a bad idea.

Why does midazolam appear to protect against adverse effects?

Even more interesting is the possible harm caused by atropine.

Why would atropine increase the rate of adverse events?


Why do we give atropine to children?

To prevent ourselves from being able to see the effects of hypoxia on the child’s heart rate.


We give children atropine to prevent their heart rates from dropping when we are doing things that are expected to occasionally result in hypoxia.

The child’s heart rate is a great indicator that we are making the child hypoxic, but we prefer to not know about the hypoxia.

Should we also avoid pulse oximetry?

We even delay our ability to identify hypoxia with pulse oximetry by using supplemental oxygen. That doesn’t mean that we should not use supplemental oxygen, only that we should assess ventilation with a measurement that is not affected by supplemental oxygen – waveform capnography.

Atropine should not be used to keep the pediatric heart rate from responding to hypoxia.

The way to prevent pediatric bradycardia is to prevent hypoxia, not to put lipstick on the hypoxia.

Image credit.

What hypoxia? No hypoxia here. Just a pulchritudinous paramedic.

Atropine is also used as an antisialog, which means that it decreases salivation. That can be an appropriate use, but if the atropine prevents the recognition of hypoxia, some saliva in the mouth may not be that important or we should use suction (just as the dentist does).

However, the study was not designed to look at that and the numbers never reached statistical significance. Does that mean that we should continue to use atropine for something that is not beneficial?

Where is the evidence that there is any benefit to anything other than the ego of the person pushing the atropine?

Oh, look! Better numbers on the monitor.

We should not be harming our patients with drugs.

To be continued in Part II, which looks at the actual IM vs. IV results.

Thank you to Peter Canning, of Street Watch: Notes of a Paramedic, for this journal article.


[1] Serious adverse events during procedural sedation with ketamine.
Melendez E, Bachur R.
Pediatr Emerg Care. 2009 May;25(5):325-8.
PMID: 19404223 [PubMed – indexed for MEDLINE]

Melendez E, & Bachur R (2009). Serious adverse events during procedural sedation with ketamine. Pediatric emergency care, 25 (5), 325-8 PMID: 19404223


The 4 ‘Ws’ of Pain Management – a discussion at First Few Moments

On the latest First Few Moments[1], Kyle David Bates hosts Brad Buck, who through an unfortunate Skyping accident we lost, Wilma Vinton, Roland Rolfsen, Dr. Laurie Roming, and me in a discussion of the Who, What, When, and Why of pain management. Being my usual difficult self, I also mention the Where of pain management –

Too often, when I have called for pain medicine orders, the medical command doctor has asked me how far I am from the hospital. How is that relevant? Unless the patient is unstable, I am generally not moving the patient until after the pain is managed. For example, some abdominal pain is made much worse with movement, while other abdominal pain is not affected by movement.

Is it appropriate to move a stable patient before managing their pain, if the movement is going to make the pain worse?

Is EMS transport with insignificant treatment?


Is EMS treatment with insignificant transport?

No. One of the ways we can make pain much worse is by driving carelessly. We do not need to transport quickly. I have transported patients at less than 15 MPH with the emergency lights on – obviously not with the siren on, since that would not be good for the patient.

Is EMS both transport and treatment?

Sometimes EMS is just transport and sometimes EMS is just treatment. Downplaying the treatment and downplaying the transport are both mistakes.

Some points that were mentioned –

1. There is no evidence that anyone can tell the difference between someone who is a drug seeker because of severe pain (kidney stones, tumor, et cetera) or someone who is a drug seeker because the person who is trying to get high.

If we do get any training on this in EMS, it is probably just a bunch of mythology. What are the instructors basing their methods on? How do they know that the patients they claims were faking actually were faking? There is a great article on this topic at Academic Emergency Medicine.[2]

2. Medication is not the only method of pain management.

3. Nitrous oxide and ketamine have different side effects from opioids.

4. Sometimes adding a sedative works much better than just giving more opioid.

5. Even hypotensive patients can be safely treated with pain medicines.

There was a 47% chance that a hypotensive patient would no longer be hypotensive after a dose of fentanyl.

the safety of fentanyl as demonstrated in the current study may be related to more conservative dosing in unstable patients, but the parallel message is that experienced EMS crews are able to exercise judgment in determining which patients should receive cautious drug dosing.[3]

Should we assume that there is no judgment going into the dosing of patients?

experienced EMS crews are able to exercise judgment in determining which patients should receive cautious drug dosing.

When should we expect hypotension after giving a dose of fentanyl?

When the patient is already hypotensive.

I have written more about this study.[4]

Go listen to the podcast.


[1] The 4 ‘Ws’ of Pain Management: a discussion – Episode 40
First Few Moments
13 Jul, 2012

[2] Truth hurts.
Veysman BD.
Acad Emerg Med. 2009 Apr;16(4):367-8. Epub 2009 Mar 6. No abstract available.
PMID: 19298618 [PubMed – indexed for MEDLINE]

Free Full Text at Academic Emergency Medicine

[3] Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia.
Krauss WC, Shah S, Shah S, Thomas SH.
J Emerg Med. 2011 Feb;40(2):182-7. Epub 2009 Mar 27.
PMID: 19327928 [PubMed – in process]

Full Text PDF Download at medicalscg.

[4] Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia
Rogue Medic
Fri, 27 May 2011

Chart Version – Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia
Rogue Medic
Sun, 05 Jun 2011

Safety of prehospital intravenous fentanyl for adult trauma patients
Rogue Medic
Thu, 03 May 2012