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

- Rogue Medic

D10 in the Treatment of Prehospital Hypoglycemia: A 24 Month Observational Cohort Study

ResearchBlogging.org
 

Why treat hypoglycemia with 10% dextrose (D10), rather than the more expensive, potentially more harmful, and less available, but traditional treatment of 50% dextrose (D50)? Why not? The only benefit of 50% dextrose appears to be that it is what people are used to using, but aren’t we used to starting IVs (IntraVenous lines) and running fluids through the IVs?

We should be much more familiar with running in fluid, than in pushing boluses of syrup.

What happens when we have temporary shortages of 50% dextrose? Do we stop treating hypoglycemia? Are we supposed to panic, because we can no longer follow tradition? No. We give the more appropriate, and lower, dose of the much lower concentration of dextrose. We provide better care because of our need.
 

Despite the traditional use of D50, there is a minimal amount of data to support it as the standard of care.[1]

 

Is 10% dextrose the perfect treatment for hypoglycemia? No, but it does appear to be less likely to cause harm than the current overtreatment with 50% dextrose.
 

Seven patients had a drop in blood glucose after D10 administration, all of 10 mg/dL or less except for one patient with a drop of 19 mg/dL who had an insulin pump infusing that was not removed by EMS personnel during D10 infusion.[1]

 

Is that any different from what happens with 50% dextrose? If this is different from D50, how does the potential harm from giving too much dextrose to most hypoglycemic patients compare to the potential harm of giving a first that is too small to fewer than 1% of hypoglycemia patients?
 

There were no reported adverse events related to dextrose infusion. Six patients who received intravenous D10 were pronounced dead in the field during the period of study. On investigator review, all patients had altered level of arousal or were in cardiac arrest prior to arrival of EMS personnel and their deaths were deemed to be unrelated to dextrose administration.[1]

 

Dextrose does not reverse death, so there is no reason to expect a better outcome for dead patients with a higher concentration of a drug that does not reverse death. Go read the excellent review of the evidence on hypoglycemia, death, and the potential of dextrose to improve outcomes from death.[2]

But is 10% really better? We don’t have any good research, but is there any good reason to give all 25 grams of dextrose in a syringe of 50% dextrose if the patient wakes up before the full dose has been administered? Would we continue to give the entire syringe of morphine, or fentanyl, or most of the other drugs that we give, if our assessment shows that the patient no longer meets the protocol criteria for administration of the drug?
 


 

76% of patients received only 10 grams of dextrose, rather than the usual 25 grams. While it is not known if any of these patients required any further dextrose, or oral glucose, while in the hospital, they should have been awake enough to take any further dextrose orally, as they would the rest of the time.

23% of patients received only 20 grams of dextrose, rather than the usual 25 grams.

Fewer than 1% of hypoglycemia patients received a dose as large as we traditionally give.
 

We do not appear to be concerned with harm from administering more aggressive treatment than is justified by the evidence.

We do appear to be concerned about our anxiety of deviating from the traditional too much is not enough approach to hypoglycemia.

Footnotes:

[1] D10 in the Treatment of Prehospital Hypoglycemia: A 24 Month Observational Cohort Study.
Hern HG, Kiefer M, Louie D, Barger J, Alter HJ.
Prehosp Emerg Care. 2017 Jan-Feb;21(1):63-67. doi: 10.1080/10903127.2016.1189637. Epub 2016 Dec 5.
PMID: 27918858
 

Of the 1,323 patients administered D10 during the study period, the 452 patients excluded from the study cohort for the aforementioned reasons were similar demographically to the study cohort. The median initial blood glucose was the same at 37 mg/dL and the median age was also 66. There were slightly more women at 229 (51%) in the excluded group compared to the cohort.

 

[2] Using Dextrose in Cardiac Arrest
Wednesday, March 14, 2012
Mill Hill Ave Command
Dr. Brooks Walsh
Article

Hern, H., Kiefer, M., Louie, D., Barger, J., & Alter, H. (2016). D10 in the Treatment of Prehospital Hypoglycemia: A 24 Month Observational Cohort Study Prehospital Emergency Care, 21 (1), 63-67 DOI: 10.1080/10903127.2016.1189637

.

Does use of Lights and Sirens save lives?

AmboLights
 

A recent Fire Chief Magazine and the current JEMS have some articles on the use of lights and sirens and the effect on patient outcomes. Doug Wolfberg, one of the EMS lawyers who might be trying to defend your choice on use of lights and sirens, states –
 

Few cows are more sacred in fire service based EMS than the ones that flash, wail and yelp. The use of emergency lights and sirens is an inseparable part of everyday EMS life.[1]

 

and –
 

Yet when we look at the actual evidence, a few things become apparent about RLS use. First, it’s proven to be dangerous. Second, it’s not proven to be beneficial.[2]

 

In another article, several of the top medical directors in the country state –
 

Unlike fire emergencies, which can grow exponentially and spread quickly, only a small subset of medical emergencies is truly time sensitive. Most don’t dramatically worsen in the course of a very few minutes, and they don’t spread from person to person.[3]

 

In rare cases, such as those where we are not able to control bleeding, or breathing, and the hospital is close enough that the patient won’t be dead by the time we get there, does use of lights and sirens save lives? In those rare cases? Sometimes.

Wouldn’t it be better to improve the quality of the people treating these patients, rather than increase the speed of transport?

When is the last time you transported a patient to the emergency department for something that needed to be done immediately to save the life of the patient?

Why not do that before transport?

Was it out of your scope of practice, did you not know what was going on, did you not feel comfortable performing the skill, could you not make up your mind about what to do, . . .?

Can’t place an endotraceal tube successfully? Use an LMA (Laryngeal Mask Airway), King Airway, BVM (Bag Valve Mask or resuscitator bag), stimulate the patient to breathe for himself, . . .

Can’t place an IV successfully? The IV is not a life line, but you can place an IO (IntraOssesous) line, apply direct pressure to bleeding, lay the patient flat (Trendelenberg does not improve things for the patient, although it might make you feel like you are doing something good), consider IM (IntraMuscular) or IN (IntraNasal) administration of medication, . . .

But it is an emergency!
 

We used to drive cardiac arrests to the hospital quickly, because we thought that was better.

We were wrong. If we do not resuscitate people prior to arrival at the hospital, they will probably stay dead. Driving fast just increases the odds that we will be as dead as the patient.

There has never been any good evidence to support driving fast.

We need to develop a better understanding of the treatment we provide. We need to provide better assessments (and continue to assess). We need to provide appropriate treatment on scene prior to transport. We need to rush less.
 

Do you believe in frequent lights and sirens transport?

Here is a dare for you.

Keep track of the times you transport with lights and sirens (these should be sentinel events) and document the actual life saving treatment provided in the emergency department in the first 10 minutes.

Keep track of this for a month, or a year.

Do you have anything?

Was it really something that saved the patient’s life?

If you do come up with something, does it amount to more than 1% of lights and sirens transports?

If we have almost always beenwrong about what is going on, should we be endangering everyone on the road to cover for our ignorance?

Footnotes:

[1] Why running lights and sirens is dangerous
Fire Chief
June 5, 2016
By Douglas M. Wolfberg, Esq.
Article

[2] Pro Bono: EMS Use of Red Lights and Siren Offers High Risk, Little Reward
JEMS
Wed, Feb 1, 2017
Doug Wolfberg
Article

[3] The Case Against EMS Red Lights and Siren Responses
JEMS
Wed, Feb 1, 2017
S. Marshal Isaacs, MD, FACEP, FAEMS , Carla Cash, MD , Osama Antar, MD , Raymond L. Fowler, MD, FACEP, DABEMS
Article

.

‘Narcan by Everyone’ Does Not Seem to be Such a Good Idea

 
Now that we have almost everyone giving naloxone (Narcan) to suspected heroin overdose patients, the fatality rate must have dropped. The panacea must have worked. My criticism of the Narcan by Everyone programs must have made me a laughing stock.[1],[2],[3],[4]

No.

Does that mean that I am a prophet and that you should worship me?

No.

Explanations exist; they have existed for all time; there is always a well-known solution to every human problem — neat, plausible, and wrong. H.L. Mencken.

I have been pointing out that the plans assumed that there would not be any unintended consequences. I explained what some of the unintended consequences would be. Many people used logical fallacies to justify ignoring the likelihood of unintended consequences. The reasonable thing to do would have been to study the implementation, so that problems would be noticed quickly.

Misdiagnosis – giving naloxone to people who have a change in level of consciousness that is not due to an opioid (heroin, fentanyl, carfentanyl, . . . ) overdose.
 

Six of the 25 complete responders to naloxone (24%) ultimately were proven to have had false-positive responses, as they were not ultimately given a diagnosis of opiate overdose. In four of these patients, the acute episode of AMS was related to a seizure, whereas in two, it was due to head trauma; in none of these cases did the ultimate diagnosis include opiates or any other class of drug overdose (which might have responded directly to naloxone). Thus, what was apparently misinterpreted as a response to naloxone in these cases appears in retrospect to have been due to the natural lightening that occurs with time during the postictal period or after head trauma.[5]

Bold highlighting is mine.

 

Failure to ventilate – not providing ventilations to a patient who is not breathing. These patients are often hypoxic (don’t have enough oxygen to maintain life) and hypercarbic (have too much carbon dioxide to maintain life). If the patient is alive, ventilation should keep the patient alive, even if naloxone is not given or if the naloxone is not effective. If the patient is dead, giving naloxone will not improve the outcome.[6]

But . . . But . . . But . . . Narcan is the miracle drug!
 


Image credit.
 

In Akron, a small Ohio city, medical examiner Dr. Lisa Kohler has seen over 50 people die of carfentanil since July. Police Lieutenant Rick Edwards says his officers are “giving four to eight doses of [naloxone] just to get a response.”[7]

 

“Every day our paramedics start CPR on someone surrounded by empty naloxone vials… people give the naloxone and walk away,” she (Ambulance Paramedics of BC president Bronwyn Barter) said in an interview.[7]

 

Where should we start?
 

All patients considered to have opioid intoxication should have a stable airway and adequate ventilation established before the administration of naloxone.[8]

 

We keep making excuses for solutions that are neat, plausible, and wrong. Why don’t we start acting like responsible medical professionals and do what is best for our patients?
 

Thank you to Gary Thompson of Agnotology for linking to this for me.

Go read Response: ‘What happens when drugs become too powerful for overdose kits’

Footnotes:

[1] The Myth that Narcan Reverses Cardiac Arrest
Wed, 12 Dec 2012 20:45:29
Rogue Medic
Article

[2] Should Basic EMTs Give Naloxone (Narcan)?
Fri, 27 Dec 2013 14:00:22
Rogue Medic
Article

[3] Is ‘Narcan by Everyone’ a Good Idea?
Tue, 03 Jun 2014 23:00:38
Rogue Medic
Article

[4] Is First Responder Narcan the Same as First Responder AED?
Wed, 18 Jun 2014 17:15:43
Rogue Medic
Article

[5] Acute heroin overdose.
Sporer KA.
Ann Intern Med. 1999 Apr 6;130(7):584-90. Review.
PMID: 10189329 [PubMed – indexed for MEDLINE]

[6] The Kitchen Sink Approach to Cardiac Arrest
Mon, 16 Feb 2015 16:00:53
Rogue Medic
Article

[7] What Happens When Drugs Become Too Powerful for Overdose Kits?
Dr. Blair Bigham
Oct 4 2016, 12:11pm
Article

[8] Naloxone for the Reversal of Opioid Adverse Effects
Marcia L. Buck, PharmD, FCCP
Pediatr Pharm. 2002;8(8)
Medscape (free registration required?)
Clinical Uses

.

The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

ResearchBlogging.org
 

This is a very interesting trial that may surprise the many outspoken amiodarone advocates, but it should not surprise anyone who pays attention to research.

ALPS showed that we should stop giving amiodarone for unwitnessed shockable cardiac arrest. The lead researcher is still trying to spin amiodarone for witnessed shockable cardiac arrest, even though the results do not show improvement in the one outcome that matters – leaving the hospital with a brain that still works.[1],[2],[3]

There is an excellent discussion of the study on the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia.

One problem with the study that they do not address on the podcast is that the patients in the study appear to have had time to watch Casablanca before treatment started. Here’s looking at you, while we’re waiting, kid. This is apparently unintentional one way of doing a placebo washout. If we wait long enough . . . .
 

Time from arrival to start of infusion was 87 ± 21 min for procainamide and 115 ± 36 min for amiodarone patients (P = 0.58).[4]

 

If nothing else, this demonstrates how little we need to worry about immediately pushing drugs for stable monomorphic VT (V Tach or Ventricular Tachycardia). Should we expect much from antiarrhythmic treatment?

Research shows that for stable monomorphic VT (V Tach or Ventricular Tachycardia) amiodarone is not very likely to be followed by an improvement. Only 29%[5] or only 25%[6] or only 15% within 20 minutes, but if we don’t mind waiting an hour it can be as much as 29%.[7] For those of you who are not good at math, that means amiodarone is about the same as doing nothing, only it comes in a syringe. Even though these poor outcomes ignore the side effects, they are the best evidence in favor of amiodarone, so what Kool-Aid are the advocates drinking?

Adenosine, yes adenosine the SVT (SupraVentricular Tachycardia) drug, appears to be more effective at treating ventricular tachycardia than amiodarone – and adenosine is faster and safer than amiodarone.[8]

What if the patient becomes unstable? First start an IV (IntraVenous) line. Then sedate the patient. Then apply defibrillator pads. After the patient is adequately sedated, then cardiovert. We do not need the pads on the patient first. If it takes a while to put the pads on, that is a problem with the ability of the doctors and nurses, not a medical problem.

It does not appear as if any patient received amiodarone or procainamide until after waiting in the ED (Emergency Department) for over an hour. Were some patients cardioverted in well under an hour? Probably. The important consideration is that the doctors and nurses be able to apply the defibrillator pads properly and quickly and deliver a synchronized cardioversion in less than a minute. If the patient has not yet been sedated, the cardioversion should be delayed until after the patient is adequately sedated, so the intervention that depends most on time is the sedation of the patient.
 

VT + Amiodarone Cardioversion
 

Is there a better treatment than amiodarone? Sedate the patient before the patient becomes unstable, then cardiovert. How do the MACEs (Major Adverse Cardiac Events) compare with sedation and cardioversion vs. antiarrhythmic treatment.
 

5.4 Proarrhythmia
Amiodarone may cause a worsening of existing arrhythmias or precipitate a new arrhythmia. Proarrhythmia, primarily torsade de pointes (TdP), has been associated with prolongation, by intravenous amiodarone, of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving intravenous amiodarone, TdP or new-onset VF occurred infrequently (less than 2%). Monitor patients for QTc prolongation during infusion with amiodarone. Reserve the combination of amiodarone with other antiarrhythmic therapies that prolong the QTc to patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.
[9]

 

All antiarrhythmic drugs can cause arrhythmias. In the absence of information about a specific problem that is best addressed by a specific drug (amiodarone is the opposite of specific), we should avoid treatments that have such a high potential for harm.

Amiodarone doesn’t even do a good job of preventing arrhythmias.
 

Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion.[10]

 

Is anything worse than amiodarone? Even epinephrine, yes epinephrine the inadequately tested cardiac arrest drug, has been followed by improved outcomes from V Tach after amiodarone failed.[11]
 

What is best for the patient?

Sedation, search for reversible causes, apply defibrillator pads, and be prepared to cardiovert.

Maybe sedation isn’t that important? This is by Dr. Peter Kowey, one of the top cardiologists in the world.
 

The man’s very first utterance was, “If it happens again, just let me die.”

As I discovered, the reason for this patient’s terror was that he had been cardioverted in an awake state. Ventricular tachycardia had been relatively slow, he had not lost consciousness, and the physicians, in the heat of the moment, had not administered adequate anesthesia. Although the 5 mg of intravenous diazepam had made him a bit drowsy, he felt the electric current on his chest and remembered the event clearly.

The patient’s mental state complicated the case considerably.[12]

 

How unimportant is sedation? How unimportant is consent?

For sedation, I would recommend ketamine, but etomidate was recommended in the podcast. Both work quickly and the most important obstacle to immediate treatment of a patient who suddenly deteriorates is the time to effect of sedation. Neither drug is expected to interfere with perfusion, which is the main excuse given for avoiding sedation for cardioversion.

This study is very small (not the fault of the authors), but it adds to the evidence that amiodarone is not a good first treatment for the patient.
 

Go listen to the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

 

Over the years, I have written a bit about cardioversion and the importance of sedation –

Cardioversion – I’m not doing that, you do it! – Mon, 24 Mar 2008

Cardioversion – 2010 ACLS – Part I – Mon, 25 Oct 2010

Cardioversion – 2010 ACLS – Part II – Sun, 31 Oct 2010

Cardioversion – 2010 ACLS – Part III – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part I – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part II – Fri, 12 Nov 2010

Synchronized Cardioversion Without Sedation – Part II Scallywag’s Response – Sun, 14 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part III – Tue, 16 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part IV – Wed, 24 Nov 2010

Comments on Cardioversion – 2010 ACLS – Part II – Mon, 16 Apr 2012
 

I have also written a bit about amiodarone –

Merit Badge Courses, Amiodarone, and tPA – Fri, 17 Sep 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part I – Wed, 01 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part II – Fri, 03 Dec 2010

Is Nexterone the Next Amiodarone? – Sat, 04 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part III – Mon, 06 Dec 2010

Where are the Black Box Warnings on These Drugs – I – Mon, 05 Dec 2011

Where are the Black Box Warnings on These Drugs – II – Sun, 11 Dec 2011

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia – Wed, 14 Dec 2011

V Tach Storm – Part I – Wed, 28 Dec 2011

V Tach Storm – Part II – Thu, 29 Dec 2011

Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia – Wed, 04 Jan 2012

NIH launches trials to evaluate CPR and drugs after sudden cardiac arrest – Sun, 29 Jan 2012

What Will Be the Next Standard Of Care We Eliminate – Wed, 28 Mar 2012

Happy Adenosine Day – Tue, 12 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part I – Tue, 26 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part II – Tue, 03 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part I – Mon, 02 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part II – Thu, 05 Jul 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part I – Mon, 17 Sep 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part II – Tue, 18 Sep 2012

How do we measure the QT segment when there are prominent U waves? – Thu, 13 Dec 2012

Woman with Risks for Torsades de Pointes Dying within Hours of Leaving the Emergency Department – Wed, 02 Jan 2013

Examples of Ventricular Tachycardia Caused by Amiodarone – Part I – Tue, 28 May 2013

Publication Bias – The Lit Whisperers – Tue, 11 Jun 2013

Standards Of Care – Ventricular Tachycardia – Wed, 31 Jul 2013

Footnotes:

[1] Dr. Kudenchuk is Misrepresenting ALPS as ‘Significant’
Tue, 12 Apr 2016
Rogue Medic
Article

[2] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest
Mon, 04 Apr 2016
Rogue Medic
Article

[3] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.
Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P; Resuscitation Outcomes Consortium Investigators.
N Engl J Med. 2016 May 5;374(18):1711-22. doi: 10.1056/NEJMoa1514204. Epub 2016 Apr 4.
PMID: 27043165

CONCLUSIONS
Overall, neither amiodarone nor lidocaine resulted in a significantly higher rate of survival or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia.

[4] Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study.
Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; PROCAMIO Study Investigators.
Eur Heart J. 2016 Jun 28. pii: ehw230. [Epub ahead of print]
PMID: 27354046

Free Full Text from European Heart Journal.

[5] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[6] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

[7] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

[8] Adenosine for wide-complex tachycardia – diagnostic?
Thu, 23 Aug 2012
Rogue Medic
Article

[9] AMIODARONE HYDROCHLORIDE- amiodarone hydrochloride injection, solution
DailyMed
5 WARNINGS AND PRECAUTIONS
FDA Label

[10] Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.
Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, Ceremuzyński L.
Europace. 2000 Jul;2(3):207-15.
PMID: 11227590 [PubMed – indexed for MEDLINE]

Free Full Text PDF + HTML from Europace

[11] Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia.
Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, Fontaine G.
World J Cardiol. 2012 Oct 26;4(10):296-301. doi: 10.4330/wjc.v4.i10.296.
PMID: 23110246 [PubMed]

Free Full Text from PubMed Central.

[12] The calamity of cardioversion of conscious patients.
Kowey PR.
Am J Cardiol. 1988 May 1;61(13):1106-7. No abstract available.
PMID: 3364364

Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P, & Resuscitation Outcomes Consortium Investigators (2016). Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. The New England journal of medicine, 374 (18), 1711-22 PMID: 27043165

Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J, & PROCAMIO Study Investigators (2016). Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. European heart journal PMID: 27354046

Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, & Ellinor PT (2010). Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17 (3), 297-306 PMID: 20370763

Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, & Ruskin JN (2006). Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Annals of emergency medicine, 47 (3), 217-24 PMID: 16492484

Tomlinson DR, Cherian P, Betts TR, & Bashir Y (2008). Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emergency medicine journal : EMJ, 25 (1), 15-8 PMID: 18156531

Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, & Ceremuzyński L (2000). Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, 2 (3), 207-15 PMID: 11227590

Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, & Fontaine G (2012). Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia. World journal of cardiology, 4 (10), 296-301 PMID: 23110246

Kowey PR (1988). The calamity of cardioversion of conscious patients. The American journal of cardiology, 61 (13), 1106-7 PMID: 3364364

.

Is EMS a Trade or a Profession?

 

In the current issue of JEMS, there is an article by Dr. Bryan Bledsoe that does an excellent job of identifying many of the problems with low standards in EMS – at least if the quality of care is important.
 

Also, if you will note, the welding curriculum was revised in 2011.

The paramedic curriculum was last revised in 2009. Which trades would you say have had the most changes in the last eight to 10 years? Certainly changes in EMS have occurred much more frequently and are much more significant than those that have occurred in welding.[1]

 
trade vs profession 1

 
In some places, EMS has been more aggressive in changing treatment guidelines/protocols to improve the care delivered to patients. In other places, change has been resisted.

Backboards are rarely used in the places that have admitted that we do not have any valid evidence that backboards improve outcomes, while we do have good evidence that backboards cause harm. Even more important is the evidence that manipulating the patient’s spine in order to stabilize the spine is wishful thinking that encourages us to do exactly what we claim to be trying to prevent.

High dose NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries) is becoming much more widely used for acute CHF/ADHF (Acute Decompensated Heart Failure), because high dose NTG dramatically improves survival and decreases the perceived need for aggressive airway manipulation.

Likewise, furosemide is being eliminated from the CHF/ADHF guidelines/protocols, because furosemide does not do what it is supposed to do and furosemide causes harm that it is not supposed to cause.

Ketamine is becoming the drug for many indications. Ketamine may be the best sedative, best analgesic, best agitated delirium treatment available to EMS.

How do we know that we have been harming patients?

Enough people stopped listening to the old timers, the QA/QI/CYA people who don’t understand quality, the brand new if it were dangerous, it wouldn’t be in the protocol people, and other opponents of quality care.

People are paying more attention to the evience, rather than making excuses for the absence of evidence.
 

What is important is whether or not the graduating paramedic is competent and ready to assume the important role of prehospital care.[1]

 

Many states use the NREMT (National Registry of EMTs) test to determine if a paramedic is ready to become a new hire paramedic with no experience, some day to be able to work without a supervisor present. Some states continue to require this babe in the woods test of outdated material as their goal for even experienced paramedics.

The NREMT is holding EMS back.
 

It is time for the national standard curriculum to go away. We must meet and decide what the core competencies of a paramedic will be. We must validate these core competencies through scientific study. Then, we should leave it up to the educators to determine how best to educate their students in these core competencies.[1]

 

The paramedic curriculum, revered by the NREMT, harms patients.

Why are we protecting a curriculum that harms patients?

Footnotes:

[1] Is EMS a Trade or a Profession?
Thu, Jul 28, 2016
ByBryan Bledsoe, DO, FACEP, FAAEM, EMT-P
JEMS Editorial Board member
Journal of EMS (JEMS)
Article

.

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

ResearchBlogging.org
 

This study is interesting for several reasons.

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

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

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

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

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

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

 

What did they find in the study?

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

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

 

The EMS approach to naloxone still appears to be –
 


Image credits – 123
 

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


Click on images to make them larger.
 

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

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

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

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

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

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

 

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

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

Footnotes:

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

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

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

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

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Fall With Dementia and No Change from Baseline Mental Status

ResearchBlogging.org
 

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

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

What can help us decide?
 

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

 

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

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

 

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

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

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

 

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


 

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

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

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

 

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

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

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

 

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

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


 

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

Footnotes:

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

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

.

Details on the Recent Patient Prematurely Pronounced Dead


 

Recently, I wrote about a patient who was declared dead by EMS, but was found to be alive by the coroner.[1],[2] Some details have been released about the circumstances.
 

“I think my wife has died,” Tygart’s husband is heard telling a Bluegrass 911 dispatcher on an audio recording of his call. “She’s not responding. I just woke up about five minutes ago. She’s in the floor. I was hollering for her and she’s in the floor. And she’s cold and she’s not doing anything.”[3]

 

Not an unusual call, but nothing to discourage a full assessment.
 

“Do you want to try CPR on her?”
“I already have. I don’t know how long she’s been laying in the floor.”
[3]

 

Unresponsive to CPR seems further evidence of death, but what do we know about anything that we hear over the radio/telephone?

Accuracy is not a strong point. Dispatchers have this problem, too. They are trying to obtain important information from a stressed called in as short a time as possible, then relay that information to EMS. It should be surprising when they get a lot of accurate information about an unstable event from someone who is not a repeat caller.

Do we base our treatment on the information from dispatch?

No. We should bring in extra equipment, but we should only use it if our assessment indicates that we should.

What about assessment?

We can certainly prioritize parts of our assessment based on information from dispatch, but we should probably not eliminate assessment based on what dispatch tells us.

After 3-4 minutes on scene, the medic calls for a coroner and cancel the ambulance.
 

Shortly after the deputy sheriff and Deputy Coroner Floro arrive on the scene, the deputy sheriff calls back to dispatch — about 30 minutes after Tygart’s husband first called — “We (inaudible) need a West Lincoln ambulance back on-scene ASAP at this time.”[3]

 

 

While the ambulance was en route, the dispatcher called Floro to find out what happened at the scene.
“What did you do? Go up there and lay healing hands on her or something?” the dispatcher asks on the recording.

“No, she was breathing before I even touched her,” Floro says.

The dispatcher asks about “1200” (the medic) calling for a coroner.

“I know, but he didn’t have a truck and he didn’t have a monitor,” Floro says. “She had no pulse and she had extremely faint breath sounds and she was over in between a bed and a wall … I couldn’t tell she was alive until we pulled her out from the bed and I could see her and I heard breath sounds.[3]

 

No monitor, but he is a medic?

If I do not have a monitor, and the rest of my ALS equipment with me, I should not be identifying myself as a medic. I am only able to respond at the BLS level, or the AFA (Advanced First Aid) level. We are not our tools, but we are not able to even fully assess patients without a full set of tools.
 

Apparently, she was cold and did not have palpable pulses, but that does not mean that a person is dead.

Since the coroner determined that she died of a subdural hematoma, there may not have been anything that could have been done if she had been treated immediately, but hypoxia is not good for head injuries either.

Was there something that gave the impression of rigor mortis?

Until the Kentucky Board of EMS finishes its investigation, we will not have all of the information. Even after the investigation, KBEMS may not release all of the information.

Footnotes:

[1] She’s Not Quite Dead Yet
Fri, 25 Apr 2014
Rogue Medic
Article

[2] WKYT Investigates: Can paramedics declare someone dead?
Sun, 27 Apr 2014
Rogue Medic
Article

[3] Lincoln Paramedic Called For Coroner While Woman Was Still Alive
Posted: Tuesday, April 29, 2014 10:33 am
By Ben Kleppinger
Article

.