Guest Post - Perhaps Paramedics Should NOT Intubate!

What if we're wrong? What if the "gold standard" for airway management is not approriate for EMS personnel? Even though many of us spent  untold hours training to perform ET intubation, and have felt justifiable pride in performing this skill well, is it possible that our efforts have been (ahem) misplaced?

This is a guest post by Ben Dowdy, NRP, exploring this unpopular position, reevaluating the opposite perspective. This is part of the inaugural "What-if-We’re-Wrong-a-Thon" organized by Brandon Oto of EMS Basics fame (and soon-to-be lead author in a Very Important Journal).

The continued role of endotracheal intubation as a standard prehospital skill continues to be debated, sometimes hotly.  I’m going to present an argument against prehospital endotracheal intubation.

Aspiration Prevention

Proponents of endotracheal intubation often use the argument that ET intubation protects the airway from aspiration.  But how true is such a claim?  Multiple studies of emergency airway management list aspiration as an infrequent complication ^1,2, only occurring 2.8-3.5% of the time.  A study of prehospital RSI³ found that pre-intubation evidence of aspiration was noticed in a significant number of patients, but only one incidence of peri-intubation aspiration was recorded, and no instances of post-intubation aspiration were reported.

What to make of this?  Aspiration pneumonia is a serious diagnosis, conferring an adjusted 2.3 odds ratio in favor of mortality⁴.  But for the majority of patients having their airway managed in the prehospital field, if aspiration is going to occur, it’s extremely likely that it happens prior to EMS providers arriving and managing the airway.  A prehospital ET tube prevents aspiration very uncommonly.

No Mortality Benefit

As EMS evolves, we’re constantly being challenged to ensure that our treatments and procedures have meaningful, patient-oriented outcomes.  As I heard it referred to early in my paramedic career, “we should be doing things for patients, not to them.”  For prehospital intubation, unfortunately, that does not appear to be the case.  The available literature investigating prehospital intubation’s effects on mortality^5-9 overwhelmingly show that if trauma patients are alive when they’re intubated in the field, their chance of dying just increased.  For patients who are already in cardiac arrest, evidence is conflicting as to whether ANY advanced airway management improves mortality, and even then the champion between supraglottic airways and endotracheal intubation varies with almost every new study that comes out.

Can EMS Education Programs Assess Competency in Intubation?

Initial requirements for intubation training in EMS used to be laughable under the National Standard Curriculum; 5 intubations was all you needed, compared with 50+ in medical schools.  The National EMS Education Standards thankfully replaced this with the more blanket term of “demonstrating competency” during providers’ initial training programs, allowing educational institutions to set the bar higher to ensure that new paramedics could competently intubate patients.  However, this higher standard has created difficulties.  A series of surveys¹⁰ distributed by the Committee for Accreditation of EMS Programs (CoAEMSP) found that 53% of programs have difficulty obtaining access to ORs for students to practice; 81% use high-fidelity simulators to determine competency and 90.7% urged CoAEMSP to allow these simulators as a means of demonstrating competency.  In others words, most EMS education institutions can’t ensure that their paramedic graduates will ever intubate an actual person, even a stable one undergoing elective surgery, prior to getting their certification or licensure.  To add even greater concern, the available airway mannequins commonly used in EMS airway training (including the ones that most programs want to use to “prove” competency) correlate extremely poorly with airway measurements of actual people¹¹.

Summary

Endotracheal intubation is a skill that’s difficult to master; it takes a lot of realistic practice during initial education and at frequent intervals afterwards to be able to succeed in prehospital settings.  Our education institutions can’t guarantee that providers entering the field can competently intubate patients.  The common argument of “aspiration protection” is a false one; aspiration doesn’t occur very often at all during emergency airway management, it occurs before we ever show up.  When we intubate people, their mortality rate increases.  It’s time to stop using endotracheal intubation as a first-line airway management technique until we can prove that we’re doing it for our patients, instead of to them.

References

1.     Thibodeau LG, et al (1997).  “Incidence of Aspiration after Urgent Intubation.”  Am J Emerg Med. 1997 Oct;15(6):562-5.

2.     Martin LD, et al (2011).  “3,423 emergency tracheal intubations at a university hospital: airway outcomes and complications.”  Anesthesiology. 2011 Jan;114(1):42-8.

3.     Vadeboncoeur TF, et al (2006).  “The ability of paramedics to predict aspiration in patients undergoing prehospital rapid sequence intubation.”  J Emerg Med. 2006 Feb;30(2):131-6

4.     Lanspa MJ, et al (2015).  “Characteristics associated with clinician diagnosis of aspiration pneumonia: a descriptive study of afflicted patients and their outcomes.”  J Hosp Med.  2015 Feb; 10(2):90-6.

5.     Evans CC, et al (2013).  “Prehospital non-drug assisted intubation for adult trauma patients with Glasgow Coma Score less than 9.”  Emerg Med J. 2013 Nov;30(11):935-41.

6.     Karamanos E, et al (2014).  “Is prehospital endotracheal intubation associated with improved outcomes in isolated severe head injury?  A matched cohort analysis.”  Prehosp Disaster Med. 2014 Feb;29(1):32-6.

7.     Taghavi S, et al (2014).  “Prehospital intubation does not decrease complications in the penetrating trauma patient.”  Am Surg. 2014 Jan;80(1):9-14.

8.     Kempema J, et al (2015).  Prehospital endotracheal intubation vs. extraglottic airway device in blunt trauma.”  Am J Emerg Med. 2015 Apr 29.

9.     Stockinger ZT, McSwain NE Jr. (2004).  “Prehospital endotracheal intubation for trauma does not improve survival over bag-valve-mask ventilation.”  J Trauma. 2004 Mar;56(3):531-6.

10.  Kalish, MA (2013).  “Definition of Airway Competency.”  http://coaemsp.org/Documents/Airway-Competency-Kalish-2013-09.pdf

11.  Schebesta K, et al (2012).  “Degrees of reality: Airway Anatomy of High-fidelity Human Patient Simulators and Airway Trainers.”  Anesthesiology.  2012 June;116(6):1204-9.

Bio: Ben Dowdy B.S., NRP, is a paramedic and EMS educator currently working in northern Idaho.  His past experiences include working as a paramedic, tactical paramedic, and SAR medic in urban, rural, and wilderness areas, including Yellowstone National Park, and teaching EMS topics for a university-based EMS education program, as well as across the US and abroad for Wilderness Medical Associates.

Update: Cyanokit for cardiac arrest in fire victims

I had written about this topic last year, but a recent EM:RAP segment and ensuing Twitter discussion prompted me to revisit the issue. Sadly, there is no new evidence to add to the discussion.  Nonetheless, let's revisit the question: 

If a pulseless patient is pulled from a smoky, burning building, will giving Cyanokit during CPR help?

 

Step 1

1. There is no known “50% ROSC rate” because of Cyanokit.

The four studies looking at this issue are, by design, unable to support any such conclusion. They were case-series, with no controls whatsoever. They gave Cyanokit to a number of people, and some of them lived. However, we have no idea if the “save rate” was better or worse than usual care. These studies show that EMS can administer Cyanokit, but they can’t speak to its effectiveness at all.  As a result, even toxicologists don’t make much of these studies.

Furthermore, most of the “saves” in one study had ROSC before they received the Cyanokit. It isn’t clear in the other studies when the patients received the antidote, and the amount of missing data makes it hard to interpret.

Go read the original studies; the links are at my post Does Cyanokit save lives in cardiac arrest? 

Step 2

2. Meds, in general, don’t increase save rates in cardiac arrest.

Although the AHA teaches a “reversible cause” approach to arrest, this isn’t helpful most of the time. For example, although heroin OD and severe hypoglycemia may cause cardiac arrest, there is no AHA recommendation to give naloxone or dextrose in cardiac arrest. In fact, naloxone use is discouraged.

Same with tPA. An AMI or a PE commonly triggers cardiac arrest, and tPA could theoretically “treat the cause.” But the evidence showed that, overall, it didn’t work during cardiac arrest. True, many of us have tried it once or twice, but not routinely. 

Step 3

3. I’m no EBM diehard, but we have to do better than this!

The evidence for Cyanokit is sort of like the evidence that supported Digibind (for digoxin OD) or fomepizole/Antizol (for methanol/ethylene glycol OD). Neither one of those drugs had a supporting RCT, or even a strong case-control trial. Indeed, the important studies showing their benefit were open-label, and uncontrolled. (E.g. Brent 1999 “Fomepizole for the Treatment of Ethylene Glycol Poisoning,” and Antman 1990 “Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments.”). 

However, the low rate of adverse effects, and the strong mechanistic and animal data, along with the difficulty of conducting a true RCT, argued strongly in favor of using these drugs, despite active discussion regarding the costs. So it’s appealing to use a similar argument to support using Cyanokit.

This argument, however, also suggests that recommendations for the routine administration of Cyanokit are very premature. The studies of Digibind and Antizol were of far higher quality than the 3 French and 1 Texas Cyanokit studies. 

For example, both Brent 1999 and Antman 1990 used prospective collection of data (rather than chart review), and both used clear, quantitative criteria for the use of the antidotes. That approach generated high quality data, which could be used to make valid comparisons with historical cohorts. By contrast, the Cyanokit studies are of very low-quality, based on chart reviews with unclear methods, and have plenty of missing data. 

Step 4

4.  Cardiac arrest at fire scene, especially in a firefighter?

It’s probably an MI, and the key issue isn’t getting a miracle drug started, but getting access to the patient to start high-quality CPR, and defibrillating as early as possible. Getting the gear off a “downed” firefighter requires a coordinated team effort, with plenty of practice beforehand.

Step 5

"Pit crew" style CPR has been proven to save lives. Firefighters have been shown to have high rates of cardiac disease, and high rates of on-duty arrests. It's a fact that it's hard to do CPR on someone wearing bunker gear and a SCBA. If your FD isn't drilling for this scenario, an expensive drug isn't going to help. 

The good news about saving a firefighter's life is that it's free and proven - but you have to put in some effort. Check out the Firefighter Down- CPR website for the specifics on how to improve your response. Here's the vid:

For better pain control, add a benzo? (Part 2 - Chest pain)

In my last post, I reviewed a recent study that demonstrated that adding a benzodiazapine (or "benzo") to morphine didn't seem to help in treating traumatic pain, and may increase the rate of side effects. But what about atraumatic pain? Specifically, what about chest pain?

Well, at least chest pain from suspected cardiac ischemia...

You can probably skip the ECG in this case.

So, could adding Ativan or Versed help when treating chest pain?

Background
There are some good reasons to think that controlling anxiety, and not just pain, would help in the treatment of patients with acute coronary syndrome, and especially STEMIs. For example, anxiety during an MI can cause an increased heart rate, and thus worsen oxygen demand, and so potentially worsen the cardiac ischemia. 

So, if we give beta-blockers to address this issue, why not treat the problem right at the root?  

A review from 2003 looked over the basic science, a few small clinical trials, and also the side effect profile of using diazepam or similar agents in acute or subacute ACS. The conclusion was pretty enthusiastic about using benzos, describing the potential risk-benefit ratio as very favorable.

"In conclusion, the authors disagree on whether the chief benefit of adding
benzodiazepines is tasting great, or in being less filling."

The studies they reviewed, however, were small, had conflicting results, and didn't apply to EMS very well. Fortunately, our Swedish friends stepped up to the plate, and conducted a randomized prehospital trial to answer this question.
 
The Study
Methods
The authors of Anxiolytics in patients suffering a suspected acutecoronary syndrome: multi-centre randomised controlled trial inEmergency Medical Service studied if adding midazolam (Versed) to standard analgesia (morphine) could help patients with chest pain. The study included EMS systems from across the Swedish region of Västra, including 500 prehospital personnel, 60 ambulances and one EMS boat.

"Squad 51 responding 11:33. KMG365"

The “usual” dose of morphine was 5 mg, while midazolam was given in 0.5 mg boluses until a total of 1-2 mg had been given. The primary outcome was the pain level at 15 minutes after the decision to give analgesia. 

Results 

After looking at the 1763 patients enrolled in the trial, they found.... no difference. Even when they looked at the subset of 599 patients who turned out to have real ACS diagnosed in the hospital, there was no benefit to adding a benzo for pain relief. 

The addition of midazolam seemed to reduce the heart rate and blood pressure to a statistically significant degree, but the clinical effect was pretty minimal.

Unfortunately, the benzo-getting patients more often became drowsy (or “dozy,” per the authors' language), much like in the trauma patients in my prior post.

Limitations

Yes, the study could have been done better. Many potential patients were not enrolled, and we don't know if they were different from the enrolled folks. Many of the secondary endpoints were vaguely defined, and not based on the patients' self-report. For example, the degree of anxiety, unlike pain, was judged by EMS personnel.

Lastly, while the trial was randomized, the EMS personal were not blinded to the study drug. In other words, EMS knew who got midazolam, and who didn't. This could have introduced some bias in the results (although I would expect it only would have made the midazolam group report better pain relief).

The Bottom Line

This trial may have had some shortcomings, but it did not suggest a clinically significant role for benzos in treating chest pain of suspected cardiac origin. So, we don't have to figure out a way to add a "B" into MONA!

For better pain control, add a benzo? (Part 1 - Trauma)

If a patient is in pain, should we also be treating their anxiety more aggressively? Some medical practitioners feel strongly that we should be.  In part 1, I'll discuss the evidence for using "benzos" (e.g. midazolam, lorazepam) for traumatic pain. The (forthcoming) part 2 will discuss using benzos to treat the pain of cardiac ischemia. 

Bourbon, for example, can treat the anxiety of MI.
Source: Not the NEJM

Trauma, pain, and benzos
Many paramedics believe that they could control traumatic pain better, and reduce morphine or fentanyl dosing, if they were allowed to add a benzodiazepine, like midazolam or Ativan. Different reasons are offered for this approach, such as the role of anxiety, the spasming of muscles in trauma, or the difficulty in controlling pain quickly with just opioids. An interesting new EMS study adds some evidence to this discussion.

The French authors of  "Does midazolam enhance pain control in prehospital management of traumatic severe pain?" enrolled patients who had a traumatic injury, and who described their pain as at least a "6" on a 10-point scale. 

All of the patients got morphine, and good doses too! The first dose was 0.1 mg/kg, and then repeat doses of 3 mg PRN every 3 minutes were administered, until the pain was down to a “3.” 

Half of these patients also received 0.04 mg/kg IV of midazolam at the same time as the initial dose of morphine, while the other half received a placebo injection.

So, did adding the benzo help? It appears not. Surprisingly, the patients who received midazolam had about the same pain relief as the placebo group. 

Unsurprisingly, they also had much higher rates of sedation: 44%, versus only 7% for the placebo group. They also found a strong trend for more hypoxia in the benzo group: 13% versus 2% for placebo. Lastly, there was no difference in the total doses of morphine given.

So, unless you're looking to "snow" more patients, this isn't a good approach!


How does this agree with other studies?

Pretty well. For example, an ED study done with kids with fractured arms also looked at morphine ± midazolam for pain control. Similar to the present study, they found no advantage in pain control, but more "drowsiness." (In the graph, "VAS" means pain level.)

The Bottom Line
When I interviewed medics for a study I did a few years ago, I was surprised to hear that many medics, from both rural and urban locations across New England, felt strongly about giving benzos for acute traumatic pain.  Here's a sample quote from one of the subjects:

Ref.

Despite having personally worked as a medic at a few of the places I visited, I was surprised to hear this perspective. Adding benzos for pain control is not common (or usually even permitted) in the emergency departments where these medics trained. 

Unless we are trying to sedate a patient, severe pain is probably best controlled with opioids only.

New thoughts on posterior MI for EMS

Many savvy medics will check the "extra" ECG leads V7 - V9 to look for a posterior MI. However, this isn't always necessary, since the appearance of leads V1 - V3 will often show sufficient evidence of an acute MI. The only two problems here are

1. Many medics don't know the classic criteria for posterior AMI.
2. The classic criteria may need to be changed somewhat!

I wrote an article about this topic a few years ago in a post at EMS 12-Lead.  A newly published case report got me thinking about this again, though! 

(Feel free to check out that link for a longer discussion.)

The Case Report
In the article "Acute Coronary Ischemia Identified by EMS Providers in a Standing Middle-aged Male with Atypical Symptoms," the authors describe the case of apatient who had syncope, followed by cardiac arrest. After the patient had ROSC, they obtained an ECG:

SOURCE

They described this pattern of anterior ST depression only as "anterolateral ischemia," but could this really be a posterior STEMI?

ECG findings - The old thinking

For years, the standard teaching on identifying a posterior MI has emphasized some common elements. Brady summarized the most important of these:

• Horizontal ST depression in V1-V4
• Tall, broad R waves (>30ms)
• Upright T waves
• Dominant R wave (R/S ratio > 1) in V2

So, a classic posterior MI should look something like:

Source

Problems with the old thinking?

The short-cut way to diagnose a posterior MI involves "flipping" the ECG. The idea is that the ST depression in the anterior leads is a "mirror" view of ST elevation in the posterior wall, and that the tall R-waves are actually deep Q-waves.

For example,  when we take the ECG above, and "flip" leads V1 - V3, it now looks like a standard STEMI.

LEFT: Unflipped - just boring ST depression
RIGHT: Flipping reveals an exciting STEMI. It's Magic!

So, our "classic" posterior, when it is flipped, looks like a STEMI. 

There is one problem though. The flipped ECG shows a big Q-wave, and the T-wave has started to invert. Usually, these findings aren't found in the early , acute stages of a STEMI.

Evolution of ECG in STEMI (source)

Instead, this pattern of Q-waves and T-wave inversion suggests an AMI that has been progressing for a few hours.

ECG findings - The new thinking
This problem - that a classic posterior STEMI looks like a subacute or old MI - was described by the authors of Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. These 13 cardiologists agreed that the old definition of posterior MI, that relies on tall R-waves and upright T-waves in leads V1 - V4, describes

"... the late “mirror image” of fully evolved ST-segment MI (STEMI) (Q waves with terminal T-wave inversion) and not the acute phase of STEMI."

They do not propose a better definition of a posterior STEMI ECG pattern. They do, however, offer this example of an ECG that better illustrates a truly acute posterior STEMI, resulting from a left circumflex occlusion. Note the ST depression in V1 - V3, and no significant R-waves or T-waves.

Back to the case report!
The ECG from the case at the start of this post showed ST depression in V1 - V4, but only small R-waves, and only a hint of an upright T-wave:

This ECG does not fulfill the "Brady" criteria listed above, but if we "flip" the ECG, we see that...

LEFT: Zoom on V1-V3
RIGHT: Flipped!

... we indeed have a classic, acute-looking STEMI! And in line with this interpretation, the patient was found to have a complete occlusion of the circumflex.

The Bottom Line
We don't have a good "new" definition of posterior STEMI that is based on interpretation of the anterior leads, but it appears that the "old" definition has shortcomings. Hopefully, future research will clarify the best ways to discern a posterior MI on the standard 12-lead ECG.

Part 2: Does Cyanokit save lives in cardiac arrest?

In the last post I reviewed some key facts about hydroxocobalamin (HCB), otherwise known by its brand name Cyanokit. However, paramedics and firefighters aren't really concerned with the animal studies - they want to know if it saves human lives! 

And according to some flashy headlines, many people believe this stuff works when nothing else can.

Source

Source

Source

But these are news reports and press releases - what does the medical evidence show? 


Does HCB help in cardiac arrest due to smoke?
This is the tough hurdle for studying any toxicologic antidote, and it's especially hard to do research in this area. The events are rare, and it's usually an emergency when these poisoning occur. For these reasons, and more, there have only been a few studies of HCB in humans.

Four studies have looked at the use of HCB in smoke-exposed patients. Interestingly, 3 of them were done in France, mostly in Paris.

Just for fun, Google "Paris" and "burning."

Study #1 - All smoke exposure patients who got HCB  
The authors of the first study looked at all the patients treated with HCB over an 8-year period  for "suspected cyanide poisoning" after a smoke inhalation, usually from a house fire. It's important to understand that there was no comparison group so it is impossible to know whether the drug helped, hurt, or did nothing.

With that in mind, all 101 patients got HCB, and all were from residential house fires; about 1/3 of those were in cardiac arrest. Forty two patients died, 30 survived, and the status of 29 patients was "unknown." 

How about patients found in cardiac arrest? Of the 38 patients who where found in arrest, 21 of those had prehospital ROSC - pretty encouraging. Unfortunately,  the majority of those (19/21) subsequently died in the ICU.

This might be encouraging if we were givne some data about those 2 out of 38 patients who survived. For instance, did they get the HCB before, during, or after their cardiac arrest? Unfortunately, there are no further details. 

Study #2 - All cyanide exposures who got HCB
Just like the study above, the authors of study #2 included patients with smoke inhalation or cyanide ingestion who were treated with HCB by EMS. Since this was written by the same authors as study #1 above,  and covers mostly the same period (1995-2008), it is likely that many of these patients overlap with those in the prior study.
Out of the 161 patients studied, 61 were found in cardiac arrest. Most of these died in the field, or ended up dying in the hospital, but 5 patients lived after getting HCB from EMS!

 
That's an 8% save rate, which seems very promising, but the authors note that most of these "saves" didn't actually get HCB before they had ROSC. As they point out (my emphasis):

"Among the 61 patients in [cardiac] arrest, 5 survived without sequelae and, in particular, without neurological sequelae. Four of the 5 patients were ... discovered in cardiac arrest by the fire brigade, and spontaneous cardiac activity was obtained after cardiac massage and oxygen therapy. ...

[H]ydroxocobalamin was not responsible for the recovery of spontaneous cardiac activity in these patients."

I'll point out that the 5th cardiac arrest survivor had his age only listed as "adult," suggesting that the EMS records were incomplete, at the least... 


Study #3 - All smoke exposures, who got HCB, and who made it alive to the ICU
The last study adopted a slightly different approach. The authors performed a retrospective "observational case series" of all of the patients who who had smoke exposure, received HCB in the field, and were subsequently admitted to the ICU. 

A total of 69 patients were enrolled. Of these, 15 patients had been in cardiac arrest when EMS found them. Of these 15 patients, only 2 survived.

Hey, 2/15 is a 13% save rate, which might be really promising. Or might not be - we can't tell from the study design.

Study #4 - All smoke exposure patients who got HCB - in Texas! 
You might not have thought that Paris and Houston would have a lot in common!

You can skip Googling "Paris" and "Houston"

As it turns out, both Parisians and Texans have been using HCB for years, and a just-published abstract describes the experience of the FD in Houston. Unfortunately, the study wasn't "Texas-sized," and was actually smaller than those done in Paris.

Like the French studies, the Houston authors looked retrospectively at all the patients who had received HCB for "possible cyanide poisoning." Over a period of 4 years, 22 patients got the drug. Half of those were found in cardiac arrest, and 8/11 had ROSC "after administration of HCB."

So, awesome, right? Unlike study #2 above, the patients in cardiac arrest actually got HCB before ROSC, not after. Is this proof that HCB, given in arrest, can produce ROSC rates in almost 75% of cases? 

 Limitations of these "case series"studies
Unfortunately, we still can't say.  All of these studies were basically case series. It is very low-quality evidence, ranking just above expert opinion. You can think of such a study design as just a fancy doctor phrase meaning "a bunch of cool stories."

Why? Because there is no comparison group in any of them. Since the drug was never actually tested against another drug, let alone a placebo, we don't know if HCB helped, or did nothing. 

Heck, for all we know, it may have even hurt patients. We just don't know.

 So, what can we do with this data?
By itself, not much. HCB is a new therapy, with potential, but no solid human evidence to support when we should use it. Of course, we don't always wait for perfect evidence to come along before using drugs and therapies.

With that in mind, what should you and your teammates do the next time FD drags a patient in cardiac arrest out of a fire? Or what if one of your firefighter teammates collapses next to you during a fire?

The next post will offer some suggestions, based on better evidence, of techniques and therapies that have been shown to lives.