Paramedicine 101

Does RSI Protect Against Aspiration of Stomach Contents

Rogue Medic — Thu, 15 Mar 2012 20:45:49 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

One of the reasons we use RSI (Rapid Sequence Induction/Intubation) is to protect the airway from aspiration of stomach contents, blood, debris, and other things that might make their way into the lungs and make the patient’s already very bad day, very much worse.

Does RSI protect against aspiration of stomach contents?

We are presented with a patient who appears to need airway management.

You believe that tracheal intubation to isolate the respiratory from the gastrointestinal tract is considered to be the optimum method to prevent aspiration in at-risk patients. Limiting the time that the airway is unprotected during the induction of anesthesia is intuitively advisable and the practice of rapid sequence induction (RSI) with cricoid pressure is widely accepted as the standard of care in this setting.¹ ^[1]

When the word intuitively is used in a medical journal, that is a bad sign. The concerns about protecting the airway for anesthesia are minor concerns compared to those faced by EMS in the much less controlled prehospital environment.

As you contemplate the intervention, you wonder what evidence is available to measure the impact of RSI on the incidence of aspiration, how it should best be performed, and what is its risk-to-benefit profile.^[1]

Certainly, we should have considered this before beginning RSI, but this is a way of involving us in the care of a patient. I imagine Theodoric of York pausing during an intubation to ponder this. Naaaah!

Does this –

Image credit.

protect against this?

Image credit.

A search of the available research (2007) was performed and –

It was readily apparent that any conclusions addressing the primary question would be inadequately supported due to the limited number of studies, most of which were retrospective in nature. As well, the working definition of RSI used by researchers was variable and many of its component parts were of unproven or questionable merits.^[1]

This is not a review of whether EMS should use RSI, but of the evidence that RSI works in the ideal environment of the OR (Operating Room).

For the purpose of our review and discussion, we defined RSI as it would be conventionally carried out by practicing anesthesiologists. The technique evaluated includes preoxygenation, rapid administration of predetermined doses of both induction and paralytic drugs, concurrent application of cricoid pressure, avoidance of bag and mask ventilation, and direct laryngoscopy followed by tracheal intubation.^[1]

How many of us avoid the use of BVM (Bag Valve Mask) ventilation for preoxygenation?

If we have paralyzed the patient’s muscles to prevent stomach contents from being propelled out of the stomach, haven’t we also paralyzed the muscles that may prevent oxygen from entering the stomach?

If we are using BVM ventilation before giving paralytics, and some of that oxygen is forced into the stomach by BVM, aren’t we providing more pressure to propel stomach contents into the airway?

Can crichoid pressure decrease the amount of oxygen that enters the stomach by positive pressure ventilation?

However, a number of factors make it difficult to employ aspiration as the outcome variable in studies assessing the impact of RSI. Aspiration is rare and very large numbers of patients would need to be studied to assess the impact of RSI on its occurrence.^[1]

Is aspiration rare because RSI works to protect against aspiration?

Is aspiration rare regardless of RSI?

For practical reasons, surrogate outcomes, such as ease or success of intubation with RSI, are the most commonly reported, with successful tracheal intubation being the single most common outcome reported in clinical evaluations of RSI protocols.^[1]

Surrogate endpoints are great for the initial assessment of a treatment, but do not tell us what we need to know about whether what we are doing is actually helping patients, is of no benefit to patients, or is harmful to patients.

We need to do better than just following some old wives’ tales from a time when far less was known about patient care.

Further, many of the reports assessing RSI outcomes are simulations of RSI conducted in healthy elective populations who may not be representative of the cohorts of patients typically subjected to RSI.^[1]

In EMS, we should not be treating many healthy patients.

EMS is supposed to be providing not elective airway management, but necessary airway management.

Following our analysis of the literature it was apparent that there was no evidence available that would allow the following question to be answered: “Does RSI reduce either the incidence or the adverse consequences of aspiration during emergency airway management?” In fact, there is no study, randomized, controlled, blinded, or otherwise, that measures the impact of any intervention on the incidence of aspiration, nor is there likely to be a statistically meaningful study conducted on this issue.^[1]

This seems to prevent the study of RSI for aspiration prevention by anesthesiologists, but maybe it is still something that EMS can examine.

We are fortunate in that our patients tend to be much more nauseated by us. At least they tend to vomit on us, or around us, much more often than they do around others (maybe oncologists or gastroenterologists see more vomit than EMS).

Can we show that the attempts to prevent aspiration are more than just placebo?

How rare is aspiration in EMS?

How many patients might benefit from RSI to prevent aspiration?

Do we want to know if we are harming our patients?

Footnotes:

^[1] No evidence for decreased incidence of aspiration after rapid sequence induction.
Neilipovitz DT, Crosby ET.
Can J Anaesth. 2007 Sep;54(9):748-64. Review.
PMID: 17766743 [PubMed - indexed for MEDLINE]

Link to Abstract and Free Full Text PDF Download from Can J Anaesth

Assuming that the incidence of aspiration during emergency surgery is 0.15%,¹³ a strategy that would simply reduce the incidence by 50% would require a study of approximately 50,000 patients to confirm that benefit (one-tailed hypothesis for improved outcome, α = 0.05, β = 0.20). Thus, the strength of any recommendation favouring the use of RSI for the prevention of aspiration would be Grade D.^[1]

All we need to understand about the evidence grading system is that D is bad. The grades do not go any lower than D. D includes expert opinion, which is the least reliable evidence that should ever be considered. Expert opinion is what is behind one of the worst abuses of patients – the Standard Of Care – I’m doing it because everyone else is doing it, not because there is any good reason to believe it is good for the patient.

Science alone of all the subjects contains within itself the lesson of the danger of belief in the infallibility of the greatest teachers in the preceding generation … Learn from science that you must doubt the experts. As a matter of fact, I can also define science another way:

Science is the belief in the ignorance of experts. – Richard Feynman.

Intramuscular Midazolam for Seizures – Part VI

Rogue Medic — Wed, 14 Mar 2012 12:00:47 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

How aggressive should we be in treating seizure patients based on this large double-blind, randomized, noninferiority trial comparing IM (IntraMuscular) midazolam (Versed) with IV (IntraVenous) lorazepam (Ativan)?

Which seizure patients should be treated with benzodiazepines?

Most patients stop seizing without any treatment and benzodiazepines can cause respiratory depression, so we need to be careful.

You can’t be too careful!

Right?

status epilepticus . . . occurs in approximately 6% of visits to the emergency department for seizures. . . . Although the term “prolonged” was previously used to refer to seizures lasting 30 minutes or longer, this interval has been shortened to 5 to 10 minutes in recent studies. This change occurred for several reasons. First, almost all convulsive seizures in adults cease in less than 5 minutes without treatment; seizures lasting longer than this are more likely to be self-sustained and to require intervention.^3,4 ^[1]

We used to be much more careful. We would wait half an hour before treating seizures out of a fear of making things worse. That fear caused us to make things worse by being too careful.

5 minutes seems to be the dividing line between seizures that will stop on their own and seizures that require treatment.

Second, the longer seizures persist, the harder they are to terminate pharmacologically.⁵ ^[1]

Being too careful resulted in higher doses of medication being given, because the dose that could have worked earlier in the seizure is no longer effective. The larger dose is also not effective. A different medication may also need to be added, even though it may not be effective, because we waited too long by being too careful!.

Delaying by more than 5 minutes increases the likelihood of not being able to stop the seizure with any medication. This is far worse than the potential side effects of giving a benzodiazepine to a patient who would otherwise have his seizure resolve spontaneously.

Third, outcome tends to correlate with seizure duration even after one controls for other factors. Mortality among patients who present in status epilepticus is 15 to 22%; among those who survive, functional ability will decline in 25% of cases.⁶ ^[1]

Benzodiazepine side effects should be easily managed, even by people with just advanced first aid training – protect the airway and make sure the patient is breathing. In the absence of adequate breathing, getting the patient to talk is most effective. If getting the patient to talk is unsuccessful, painful stimulus is indicated. If painful stimulus is unsuccessful, rescue breathing is indicated.

The effects of midazolam on the CNS are dependent on the dose administered, the route of administration, and the presence or absence of other medications. Onset time of sedative effects after IM administration in adults is 15 minutes, with peak sedation occurring 30 to 60 minutes following injection.^[2]

Midazolam given IM is not metabolized as quickly as when given IV, but midazolam should still be metabolized more quickly than IV lorazepam (Ativan). Unfortunately, the label does not include information about the time to return to being alert following IM midazolam, so I can only make this apples and oranges comparison. When I have given midazolam IV, I have had to give more midazolam before arriving at the hospital (after I had given a total dose that was successful) or more sedation has had to be given the hospital (after I had given a total dose that was successful). I have never seen IV lorazepam metabolized that quickly. So midazolam is metabolized much more quickly IV, than lorazepam is metabolized IV. Unfortunately, I could not find more appropriate information to compare the metabolism of IM midazolam and IV lorazepam.

The intended effects of the recommended adult dose of ATIVAN Injection usually last 6 to 8 hours.^[3]

Image credit.

This study does show that the patients receiving IM midazolam did not end up hospitalized as often, which may be due to more rapid metabolism of IM midazolam.

the proportion of subjects admitted was significantly lower (and the proportion discharged from the emergency department was significantly higher) in the intramuscular group than in the intravenous group (P=0.01).^[4]

What is needed is a good study comparing buccal midazolam, IN (IntraNasal) midazolam, and IM midazolam to find out which works best. Perhaps a rectal diazepam group could be included to put another nail in that coffin, but rectal diazepam has the one thing going for it that no amount of evidence seems to be able to overcome – tradition. We need to stop killing our patients with tradition.

Multiple studies have shown that nasal or buccal midazolam stops seizures faster than rectal or intravenous diazepam¹³ and is absorbed faster than intramuscular midazolam.^{13 – 15} ^[1]

Buccal or IN midazolam stops seizures faster than IV or rectal diazepam, but is only absorbed faster than IM midazolam?

Footnotes:

^[1] Intramuscular versus intravenous benzodiazepines for prehospital treatment of status epilepticus.
Hirsch LJ.
N Engl J Med. 2012 Feb 16;366(7):659-60. No abstract available.
PMID: 22335744 [PubMed - in process]

^[2] MIDAZOLAM HYDROCHLORIDE injection, solution
[Hospira, Inc.]
DailyMed
FDA Label

^[3] ATIVAN (lorazepam) injection, solution
[Baxter Healthcare Corporation]
DailyMed
FDA Label

^[4] Intramuscular versus intravenous therapy for prehospital status epilepticus.
Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y, Barsan W; NETT Investigators.
N Engl J Med. 2012 Feb 16;366(7):591-600.
PMID: 22335736 [PubMed - in process]

Intramuscular Midazolam for Seizures – Part V

Rogue Medic — Tue, 13 Mar 2012 16:15:16 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

How should this large double-blind, randomized, noninferiority trial comparing IM (IntraMuscular) midazolam (Versed) with IV (IntraVenous) lorazepam (Ativan) affect the way we treat patients with seizures?

Click on image to make it larger.

21.3% of patients had their seizures stop before they could be given IV lorazepam, while none of the IM midazolam patients had seizures stop before being given medication.

Does that provide a bias toward improved outcomes with IM midazolam?

Study Outcomes
The primary outcome was termination of seizures before arrival in the emergency department without the need for the paramedics to provide rescue therapy.^[1]

Seizures were absent without rescue therapy on arrival in the emergency department in 329 of 448 subjects assigned to active treatment with intramuscular midazolam (73.4%) and in 282 of 445 assigned to active treatment with intravenous lorazepam (63.4%) (difference, 10 percentage points; 95% confidence interval [CI], 4.0 to 16.1; P<0.001 for noninferiority and P<0.001 for superiority) (Fig. 2).^[1]

The patients who had seizures stop without any lorazepam are included in those considered successfully treated.

This is appropriate, since we can expect a similar rate of spontaneous resolution among the patients receiving IM midazolam. The only difference is that those patients will have received the midazolam so quickly that the seizure will not yet have stopped.

Status epilepticus was terminated by the time of arrival at the emergency department in 59.1 percent of patients given lorazepam, 42.6 percent of patients given diazepam, and 21.1 percent of patients given placebo (P=0.001)^[2]

Is this a reason to avoid/delay administration of IM midazolam?

No.

The greater risk appears to be to the patients with continuing seizures. The primary benefit of IM midazolam is the rapid administration.

There is no evidence of any harm to the patients who would have their seizures stop without midazolam. There is evidence of harm from delaying/avoiding treatment. Most seizures will stop prior to the arrival of EMS. Delays in treatment should probably only be for those known to have self-limiting seizures and EMS is at the patient’s side in less than 5 minutes.

An out-of-hospital complication (hypotension, cardiac dysrhythmia, or respiratory intervention) occurred in 7 (10.6 percent) of the patients treated with lorazepam, 7 (10.3 percent) of the patients treated with diazepam, and 16 (22.5 percent) of the patients given placebo (P=0.08). The most common complication was a change in respiratory status requiring ventilation assistance by bag valve-mask or an attempt at intubation (7 patients given lorazepam, 6 given diazepam, and 11 given placebo).^[2]

Those who did not receive benzodiazepines did not do as well as those who did receive benzodiazepines – this includes the most worrisome side effect of benzodiazepines – respiratory compromise. We are not improving outcomes by delaying care or by using low doses.

Among subjects admitted to the hospital, the lengths of stay in the intensive care unit and in the hospital did not differ significantly between the groups, but the proportion of subjects admitted was significantly lower (and the proportion discharged from the emergency department was significantly higher) in the intramuscular group than in the intravenous group (P=0.01).^[1]

If there is no IV already in place, is there much reason to not use IM midazolam for active seizures?

No.

Our data are consistent with the finding that endotracheal intubation is more commonly a sequela of continued seizures than it is an adverse effect of sedation from benzodiazepines.¹¹ ^[1]

High dose benzodiazepines appear to be more likely to prevent intubation, than to result in intubation. This is something that many medical directors do not seem to have considered.

See also Part I, Part II, Part III, and Part IV.

Footnotes:

^[1] Intramuscular versus intravenous therapy for prehospital status epilepticus.
Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y, Barsan W; NETT Investigators.
N Engl J Med. 2012 Feb 16;366(7):591-600.
PMID: 22335736 [PubMed - in process]

^[2] 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. with link to PDF Download

Intramuscular Midazolam for Seizures – Part IV

Rogue Medic — Fri, 09 Mar 2012 13:00:19 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

What does this study mean for the treatment of patients who are having seizures?

The median time to administration of active treatment was significantly shorter by the intramuscular route than by the intravenous route (1.2 vs. 4.8 minutes), but the onset of action (i.e., termination of convulsions) occurred sooner after intravenous administration than after intramuscular administration (1.6 vs. 3.3 minutes).^[1]

Click on images to make them larger.

The good news for fans of IV (IntraVenous) drugs for seizures is that giving IV lorazepam at the same time as giving IM (IntraMuscular) midazolam will result in faster termination of seizures.

If an IV is already in place, the average time for the IV lorazepam to stop the seizure is about 1.6 minutes after the lorazepam is pushed into the IV line.

The average time for the IM midazolam to stop the seizure is about 3.3 minutes after the midazolam is injected into the muscle.

If an IV is already in place, IV lorazepam should be significantly faster.

Would IV midazolam also work faster than IM midazolam?

Probably, but that was not demonstrated in this study. My preference is to give IV midazolam, rather than IV lorazepam, because the midazolam will wear off more quickly.

I am initially much more interested in stopping the seizure, than in the side effects that might be present as a result of aggressive dosing of benzodiazepine.

After the seizure, I want any side effects to stop as quickly as possible. Midazolam is going to be metabolized much more quickly than lorazepam. In the hospital, the continuing treatment of the patient will be in the hands of the emergency physician who will have a much broader selection of medications available to treat against further seizures.

Benzodiazepines appear to be the best emergency treatment for seizures, but they may not be good for longer term treatment of the same seizures.

The problem is that EMS and ED (Emergency Department) patients rarely have an IV in place when seizures begin and it is not easy to start an IV on a patient while the patient is seizing.

Image credit.

If an IV is NOT in place, then the delay in giving the medication is both dramatic and significant enough to completely eliminate the difference in absorption that favors giving IV medication.

With average times of 1.2 minutes from opening the medication box to injecting the medication IM and 4.8 minutes from opening the medication box to injecting the IV medication, the difference is 3.6 minutes.

The IV lorazepam works 1.7 minutes faster, but it takes 3.6 minutes longer before the IV lorazepam can be given, on average.

That difference means that the IM midazolam stops the seizure 1.9 minutes faster than the IV lorazepam.

The average total time to termination of seizure after opening the medication container was 6.4 minutes with IV lorazepam.

The average total time to termination of seizure after opening the medication container was 4.5 minutes with IM midazolam.

After 4.5 minutes, the medic is still working on starting the IV, but the seizure has already stopped in the IM midazolam group.

This should not be a difficult decision.

See also Part I, Part II, and Part III. To be continued in Part V.

Footnotes:

Nontraumatic out-of-hospital hypotension predicts inhospital mortality

Rogue Medic — Wed, 07 Mar 2012 13:00:07 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

An interesting examination of something that we take for granted. Does any instance of hypotension increase the risk of death for patients with life-threatening or potentially life-threatening conditions? Hypotension is categorized as SBP (Systolic Blood Pressure) less than 100 mm Hg, rather than SBP <90.

They assessed patients with respiratory distress, syncope, chest pain, dizziness, altered mental status, anxiety, thirst, weakness, fatigue, or the sensation of impending doom.

Due to the difference in age of the groups, the non-hypotensive group was abbreviated (truncated) to match the significantly older (P<.0001, unpaired t test) hypotensive group within one standard deviation. This cut the non-hypotensive group from 2,733 to 1,362 – eliminating just over half of the group. This should do a good job of controlling for the age difference. There were two locations for the study, but the significant difference in ages was only observed at one location.

Nonexposure patients were thus priority I or II transported patients, aged 48 to 84 years, with systolic blood pressure always more than 100 mm Hg and with 1 or more of 10 predefined symptom documented.^[1]

That misrepresents the nonexposure (not hypotensive) patients. These patients did not have continual measurement of their blood pressures. A minimum of only one set of vital signs was required.

I do try to take vital signs when there is a change in patient presentation, but I have noticed that not everyone behaves as I do.

A lack of documentation of <100 SBP is not the same as systolic blood pressure always more than 100 mm Hg. Here are some of the problems with assuming that all <100 SBPs were identified by a random assessment of at least one set of vital signs –

Were vital signs assessed with every change in presentation?

Were all changes in presentation observed?

Is a drop in SBP always going to be accompanied by a change in presentation?

Is hypotension always going to be accompanied by a change in presentation?

The answers are – No, No, No, and No.

Inhospital mortality was determined by first searching the Social Security Death Index.^[1]

Is this a good method of differentiating between living people and dead people?

If the government thinks I am alive, that does not mean that I am alive. If the government thinks I am dead, that does not mean that I am dead, nor that I have a <100 SBP.

Secondary analysis measurements were the relationship between age and inhospital mortality in hypotensive patients, the relationship between the initial out-of-hospital systolic blood pressure and inhospital mortality, the inhospital mortality rate of transient versus sustained hypotension, and a calculation of the sensitivity and specificity of out-of-hospital hypotension for inhospital mortality.^[1]

At one site, SBP from 91 to 99 appears to improve survival. This may be just the law of small numbers at work. Those with transient hypotension are probably going to have blood pressures that are close to the dividing line.

Venue 2 has similar results, except here there are larger increases in the death rates at 91 – 99 and <70.

The sustained low blood pressure appears to be the real danger, while transient low blood pressure does not appear to be significantly different from zero assessments of low blood pressures.

the mortality rate among these 255 patients was 33% (95% CI 27% to 39%).^[1]

The effect of a sustained low blood pressure would have been a good study to follow this study.

Is it predictive?

Does it predict something that we can reverse?

Does sustained low blood pressure mean sustained in spite of treatment?

What kind of treatment(s) would be appropriate?

Patients with a systolic blood pressure equal to 100 mm Hg were not included in the analysis; at venue 1 this was 23 patients, and at venue 2 it was 252 patients.^[1]

Those patients would have had one or more measurements of SBP = 100, but no measurements of SBP <100. 5.8% (regardless of group) at venue 1 and 3.5% of the nonexposure group at venue 2. The 252 patients would have added almost another half (47.3%) to the exposure group at venue 2.

This raises an important question.

Why is this one SBP so commonly represented as the lowest blood pressure in the vital signs?

How often will 100 be the lowest documented SBP in any group?

Is <100 only a little more than twice as likely as 100 for the lowest documented SBP?

Does documentation of <100 SBP require treatment under a different protocol/algorithm?

There were 3,128 patients at venue 1 and only 23 SBP measurements of exactly 100.

There were 7,679 patients at venue 2 and 252 SBP measurements of exactly 100.

Venue 2 has only 2 1/2 times as many patients, but 11 times as many SBP measurements of exactly 100. Were the exclusions for SBP exactly equal to 100 done before truncation and matching? We cannot tell from the information provided.

Footnotes:

^[1] Nontraumatic out-of-hospital hypotension predicts inhospital mortality.
Jones AE, Stiell IG, Nesbitt LP, Spaite DW, Hasan N, Watts BA, Kline JA.
Ann Emerg Med. 2004 Jan;43(1):106-13.
PMID: 14707949 [PubMed - indexed for MEDLINE]

Psychic vs. RAD-57

Rogue Medic — Thu, 23 Feb 2012 21:15:25 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

Continuing what I wrote Tuesday and Wednesday about the repeated failure of Masimo’s RAD-57 to correctly discriminate between CO (Carbon monOxide) poisoning and no exposure to CO.^[1], ^[2]

Given the ~~whimsical nature~~ lack of reliability of the RAD-57, should this be an example of what ambulances will look like?

Maybe I should ask a psychic.

Image credits – 1, 2, and 3.

There are two big advantages that the RAD-57 has over the psychic.

1. Many cases of CO poisoning are probably not diagnosed due to vague symptoms that go away when the person leaves the environment.

2. Sometimes the RAD-57 does seem to get it right, but only sometimes.

There is one big disadvantage of the RAD-57 compared to the psychic.

Nobody is going to send a firefighter back to fight a fire based on the word of a psychic – at least I hope not.

Firefighters are probably being screened to safety with the RAD-57.

How many hospitalized firefighters, or dead firefighters, will it take to demonstrate that the RAD-57 is not accurate enough to use to screen for CO poisoning?

MK, from Probie To Practitioner, writes –

We have the RAD-57, and I would agree that it’s a fairly unreliable device. I once put it on my finger to try it out on the way to a call, and it gave me a reading of 7%. I have never smoked a day in my life, and before getting on the ambulance, I had spent almost 4 hours doing station chores outside.^[3]

This is above the 6.6% cut-off for CO poisoning recommended in the most recent study.^[4]

Maybe MK did not use the RAD-57 correctly.

Quick and easy-to-use—requires no user calibration and does not require patient cooperation or consciousness.^[5]

While Masimo is not exactly stating that the RAD-57 is So easy a caveman could use it, ease of use and simplicity are emphasized in their sales pitch.

Claims of operator error demonstrate dishonesty on the part of Masimo.

Is the RAD-57 easy to use, or do we have to align it with the patient’s chi forces, when the moon is just right, after doing a voodoo dance?

The Masimo slogan appears to be –

Trust Masimo. It’s always operator error, never equipment failure.

Too Old To Work, from Too Old To Work, Too Young To Retire, writes –

Funny you should bring this up. A few months ago we were sent to a “possible CO leak” with mulitple patients. The only problem was the the FD got readins of 0 when they tested the air for CO. Which was confusing to say the least because the first unit on scene with a RAD 57 got a reading of 18 ppm on an elderly gentleman who had some dypnea and chest pain.

The supervisor was convinced that the FD didn’t know what they were doing because of the RAD 57 readings.

Too Old To Work goes on to provide more details in the rest of his comment.^[6]

The problem identified in the Touger study was that the RAD-57 was not sensitive enough. The Rad-57 missed most of the actual cases of CO poisoning.^[7] The solution seems to be to increase the sensitivity to the point where saying, Carbon monoxide, will set it off.

The question still unanswered is –

How many cases of CO poisoning does the RAD-57 miss?

We will probably only learn this from the lawyers, because Masimo has not been providing useful information.

Footnotes:

^[1] Accuracy of Noninvasive Multiwave Pulse Oximetry Compared With Carboxyhemoglobin From Blood Gas Analysis in Unselected Emergency Department Patients
Paramedicine 101
Tue, 21 Feb 2012
Article

^[2] Mass sociogenic illness initially reported as carbon monoxide poisoning.
Paramedicine 101
Wed, 22 Feb 2012
Article

^[3] Mass sociogenic illness initially reported as carbon monoxide poisoning.
Paramedicine 101
02/22/2012 at 13:44

Comment by MK

^[4] Accuracy of noninvasive multiwave pulse oximetry compared with carboxyhemoglobin from blood gas analysis in unselected emergency department patients.
Roth D, Herkner H, Schreiber W, Hubmann N, Gamper G, Laggner AN, Havel C.
Ann Emerg Med. 2011 Jul;58(1):74-9. Epub 2011 Apr 2.
PMID: 21459480 [PubMed - indexed for MEDLINE]

Annals of Emergency Medicine podcast
Podcast Download in MP3 Format

Because a false-negative reading could have serious medical consequences, this device should be tested in a much larger number of poisoned patients to confirm the generalizability of our stated cutoff values.

^[5] RAD-57
Masimo
Product information page

^[6] Mass sociogenic illness initially reported as carbon monoxide poisoning.
Paramedicine 101
02/23/2012 at 03:00
Comment by Too Old To Work

^[7] Performance of the RAD-57 pulse CO-oximeter compared with standard laboratory carboxyhemoglobin measurement.
Touger M, Birnbaum A, Wang J, Chou K, Pearson D, Bijur P.
Ann Emerg Med. 2010 Oct;56(4):382-8. Epub 2010 Jun 3.
PMID: 20605259 [PubMed - indexed for MEDLINE]

Free Full Text Article from Ann Emerg Med with links to Free Full Text PDF Download

The RAD device correctly identified 11 of 23 patients with laboratory values greater than or equal to 15% carboxyhemoglobin (sensitivity 48%; 95% CI 27% to 69%).

Less than half?

Mass sociogenic illness initially reported as carbon monoxide poisoning

Rogue Medic — Wed, 22 Feb 2012 13:00:54 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

This is adding to what I wrote yesterday about the continuing failure of Masimo’s RAD-57.^[1] The RAD-57 does not demonstrate any kind of acceptable sensitivity or specificity to be marketed as a mass screening device – and especially not to screen firefighters to go back to fighting fire. This is just more evidence that the RAD-57 does not accurately measure carboxyhemoglobin (COHb).

Here is a report of a mass delusion that seems to have been compounded by the use of the Masimo RAD-57 non-invasive CO monitor. CO (Carbon monOxide) is a significant cause of poisoning in the US, but not relevant in this case. The RAD-57 incorrectly identified CO poisoning in half a dozen people who do not appear to have had any exposure to CO.

Sociogenic illness is a rare but well-described phenomenon. It involves a constellation of physical signs and symptoms without an organic cause in a group of individuals with a common ‘‘exposure’’ (1–8). It often occurs in the setting of large gatherings such as schools or when large numbers of people are living or working in close proximity.^[2]

I wrote about a different example of mass delision a couple of weeks ago.^[3] We underestimate our ability to delude ourselves, but we are great at self-delusion and we are most delusional in groups. No need for any objectivity. Just go with the feeling of a group.

Approximately 15 min into the mass, one child fainted, followed by another child. The children did not have any seizure activity and immediately awoke with normal mental status and were removed from the church. Within minutes, several more children reported a variety of complaints, including nausea, hand paresthesia, and dyspnea.^[2]

A poison strong enough to cause people to pass out, is not going to result in a return to normal mental status right away.

The ﬁre department initially evaluated the patients with complaints, including obtaining carboxyhemoglobin (COHb) oximetry and oxygen saturation readings from a hand-held portable Masimo^® device (Masimo Corporation, Irvine, CA). At the scene, 6 patients were reported to have elevated COHb levels. As such, the church was closed and paramedics, as well as the city’s hazardous materials (HAZMAT) team, were called to the scene.^[2]

If only someone had told them that the RAD-57 doesn’t work, much of the chaos could have been avoided.

Image credit.

Blood COHb levels, obtained in all patients soon after arrival in the ED, ranged from 0.2% to 1.2% (mean 0.65%). The hospital laboratory reference range for COHb is < 1.5% for non-smokers and as high as 5% for smokers. However, this upper value can be much higher in heavy smokers (9). None of our patients had elevated blood COHb levels.^[2]

A magic diesel cure?

It’s a miracle!

In the ED, all patients had normal physical examinations, including neurologic and respiratory examinations.^[2]

Were their physical exams much different on scene?

Subsequent evaluation of the church, classrooms, and surrounding premises by ﬁre department and HAZMAT personnel found no evidence of carbon monoxide or any other toxicants.^[2]

The interesting part that is not well described is the initial response of the fire department. Almost always, they have atmospheric CO alarms on their gear. When a firefighter walks into a room with elevated CO, the alarm goes off. When there is a report of a possible CO exposure, a couple of fully geared up firefighters will investigate everywhere they can in a building, looking for areas where CO might be leaking and for areas where CO might have accumulated.

There is no mention of any finding of CO at any time on scene.

No – the RAD-57 is not an indication of the presence of CO.

The affected persons were sitting in various areas of the church and many of the unaffected individuals were sitting near affected persons. This variability is not consistent with a simple asphyxiant. Furthermore, several patients became symptomatic after leaving the church, which would not be seen with a simple asphyxiant.^[2]

Exposures to gasses should present with a predictable pattern. The people in the most heavily concentrated area should be the most affected, with the smallest people (generally children) and the most active people (also generally children) being more affected than the larger and less active people. That was not the case. This suggests MSI (Mass Sociogenic Illness, or mass delusion).

the escalation of symptoms and increased number of persons affected along with increasing ﬁre and ambulance presence is a common phenomenon in MSI, referred to as ‘‘line of sight transmission.’’^[2]

Even if it appears obvious that this is a mass delusion, we should provide treatment as appropriate for the symptoms presented. In this case, some oxygen is the only treatment indicated and the only treatment provided.

I wonder if this will lead to others reporting similar cases of mass delusions compounded by ~~Magic 8 Ball~~ RAD-57 readiongs.

Accuracy of Noninvasive Multiwave Pulse Oximetry Compared With Carboxyhemoglobin From Blood Gas Analysis in Unselected Emergency Department Patients

Rogue Medic — Tue, 21 Feb 2012 23:10:44 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

The Masimo RAD-57 non-invasive CO monitor is promoted as an accurate way to identify patients at risk of life-threatening complications of CO poisoning. CO (Carbon monOxide) is a significant cause of poisoning in the US, with hundreds of fatalities each year.

Masimo claims that their RAD-57 is able to accurately measure blood levels of CO without any complicated lab equipment. If it works, the RAD-57 might save some lives. Unfortunately, the research that has not been funded by Masimo does not support a decision to buy a RAD-57 until after they improve the device.

Suspicion of CO poisoning is very important in identifying CO poisoning. One study was conducted at a burn center among patients already suspected of having CO exposure.

The RAD device correctly identified 11 of 23 patients with laboratory values greater than or equal to 15% carboxyhemoglobin (sensitivity 48%; 95% CI 27% to 69%).^[1]

A coin flip is going to be just as accurate as a test that identifies only 48% of the affected patients.

The RAD-57 was shooting at fish in a barrel and still missed most of the time.

Dr. Michael O’Reilly (Executive Vice President of Masimo Corporation) has claimed that those researchers, who are not on the Masimo payroll, are biased against his device.^[2]

What does he understand about science, objectivity, or controlling for biases?

Nothing comes to mind.

Click here to view the video on YouTube.

Even some people who are not on the Masimo payroll have suggested that the RAD-57 might be useful and that the next study (quoted below) would confirm the usefulness of the RAD-57.

Compared with the large population used for the calculation of bias and precision, the number of patients actually found to be poisoned was small, especially in the group of poisoned smokers. Therefore, the opportunity for false-negative results was limited. Because a false-negative reading could have serious medical consequences, this device should be tested in a much larger number of poisoned patients to confirm the generalizability of our stated cutoff values.^[3]

This does not contradict the first study.

What is the problem?

Symptoms of CO poisoning are nonspecific, ranging from mild headache, nausea, confusion, and dizziness to end-organ injury such as myocardial infarction,⁶ stroke,⁷ and death. ^{[8] and [9]} Diagnosis is therefore difficult and relies on clinical suspicion and confirmation by measurement of carboxyhemoglobin (COHb), using either venous or arterial10 blood gas analysis. However, COHb analyzers are not ubiquitously available.¹¹ As a result, many victims of CO poisoning might be overlooked and misdiagnosed. ^{[12] and [13]} ^[3]

Suspicion of illness/exposure is the most important part of identification.

If we examine patients without considering suspicion, does the RAD-57 improve identification?

Maybe, but this study is not capable of testing that hypothesis.

These are only patients who are going to have ABGs (Arterial Blood Gas measurements) regardless of what the RAD-57 shows. We don’t know how many of the patients who did not have ABGs, or did not have ABGs within one hour of RAD-57 measurement, actually had CO poisoning.

Blood gas analysis (arterial or venous) (Table 1) was performed later as a standard procedure in our ED on discretion of the treating physician for a variety of clinical reasons.^[3]

If the patient had a low reading on the RAD-57 and did not have an ABG, should we conclude that the unmeasured carboxyhemoglobin level was also low?

Of course not.

31% of patients who had ABGs were excluded because there was more than one hour between RAD-57 measurement and ABG measurement. How many of these patients were presenting as unstable and had the RAD-57 measurement omitted? How many of these patients were presenting as very stable and had the RAD-57 measurement over an hour before the ABG?

We do not know.

How many of the 17 patients in the documented sample had life-threatening symptoms?

We do not know.

Maybe all 17.

Maybe zero.

How many of the 17 patients in the documented sample had only minor symptoms?

We do not know.

Maybe all 17.

Maybe zero.

This kind of information is not included in the study.

What was the basis of diagnosis of CO poisoning?

The diagnosis of CO poisoning was based on increased COHb levels and clinical symptoms consistent with poisoning, including headache, vomiting, abdominal pain, and loss of consciousness.^[3]

Identifying 16 out of the 17 patients in the 1,578 patient sample is impressive, but when we limit the patients to those with symptoms suggesting CO poisoning, we lose any possible value of the non-invasive screening.

These are the patients who are going to have blood drawn to assess for CO poisoning regardless whether anyone uses a RAD-57.

There is no benefit to RAD-57 screening in this setting.

What about using the RAD-57 in 1,017 EMS patients, regardless of the reason for the 911 call?

Of the 11 patients with a SpCO >15%, 10 were transported to a hospital for which the investigators had institutional review board (IRB) approval to review the patient’ s medical record. Of those 10, none had confirmatory venous carboxyhemoglobin levels. The two patients with an SpCO level of 21% did have a repeat SpCO documented at triage upon arrival to the emergency department. Their repeat levels were 8% and 2%. None of the 10 patients with levels >15% ultimately were diagnosed with and treated for carbon monoxide exposure or toxicity.^[4]

The same idea, just not limited to patients chosen by having ABGs measured within one hour of RAD-57 measurement.

The result is very different.

None of the patients with elevated RAD-57 measurements had carboxyhemoglobin measured by drawing blood.

None of the patients with CO poisoning (according to the RAD-57) were treated for CO poisoning.

Is the RAD-57 reliable for determining if a patient should not go to the hospital?

Absolutely not.

What is the target audience of RAD-57 marketing?

Firefighters.

What is the patient population studied?

Patients already being treated in the hospital. They may include firefighters, but there is nothing in the study to indicate if there are any firefighters in the sample.

Quick and easy-to-use—requires no user calibration and does not require patient cooperation or consciousness.^[5]

Dr. Michael O’Reilly (Executive Vice President of Masimo Corporation) had a bunch of excuses for the study that did not agree with the research paid for by Masimo. One excuse was that incorrect use of the RAD-57 interfered with results, even though Masimo trained the people using the RAD-57. Would Dr. O’Reilly have mentioned this if the study had produced the results he wanted?

Image credit.
Trust me. I am here to serve you.

Keep Firefighters Safe From CO Poisoning

> Have CO levels tested on the scene with the Masimo Rad-57.

• Just because firefighters don’t feel like they have CO poisoning doesn’t mean that they don’t have unsafe levels of carboxyhemoglobin (SpCO) in their bloodstream.

• That’s why rehab guidelines support the use of on-scene CO testing.⁶ To be safe, have SpCO levels tested with a Masimo Rad-57 before going back into the fire and during overhaul, even if firefighters think they’re okay.

> Get prompt on-scene treatment.

• Recognition is the key to immediate on-scene treatment. With early recognition, treatment for CO poisoning can begin immediately, which significantly reduces both immediate and long-term health risks.^[6]

To be safe, have SpCO levels tested with a Masimo Rad-57 before going back into the fire and during overhaul, even if firefighters think they’re okay.

Masimo is providing very bad advice. Is Masimo trying to kill firefighters?

And if the RAD-57 does not detect CO poisoning, is that any reason to allow a firefighter to go back into a fire?

Absolutely not.

The RAD-57 should NEVER be used to screen asymptomatic people for CO poisoning.

The RAD-57 should NEVER be used to rule out CO poisoning.

Footnotes:

^[1] Performance of the RAD-57 pulse CO-oximeter compared with standard laboratory carboxyhemoglobin measurement.
Touger M, Birnbaum A, Wang J, Chou K, Pearson D, Bijur P.
Ann Emerg Med. 2010 Oct;56(4):382-8. Epub 2010 Jun 3.
PMID: 20605259 [PubMed - indexed for MEDLINE]

Free Full Text Article from Ann Emerg Med with links to Free Full Text PDF Download

^[2] Performance of the Rad-57 pulse co-oximeter compared with standard laboratory carboxyhemoglobin measurement.
O’Reilly M.
Ann Emerg Med. 2010 Oct;56(4):442-4; author reply 444-5. No abstract available.
PMID: 20868919 [PubMed - indexed for MEDLINE]

Free Full Text of letter and author reply from Ann Emerg Med with links to Free Full Text PDF Download

^[3] Accuracy of noninvasive multiwave pulse oximetry compared with carboxyhemoglobin from blood gas analysis in unselected emergency department patients.
Annals of Emergency Medicine podcast
Podcast Download in MP3 Format

^[4] Non-invasive carboxyhemoglobin monitoring: screening emergency medical services patients for carbon monoxide exposure.
Nilson D, Partridge R, Suner S, Jay G.
Prehosp Disaster Med. 2010 May-Jun;25(3):253-6.
PMID: 20586019 [PubMed - indexed for MEDLINE]

Free Full Text PDF Download from Prehosp Disaster Med.

^[5] RAD-57
Masimo
Product information page

^[6] RAD-57 for Fire/EMS
Masimo
Product information page

Intramuscular Midazolam for Seizures – Part III

Rogue Medic — Mon, 20 Feb 2012 13:50:04 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

I have already pointed out my disappointment with the references of this large double-blind, randomized, noninferiority trial comparing IM (IntraMuscular) midazolam (Versed) with IV (IntraVenous) lorazepam (Ativan). One of those criticisms appears to be just due to a typographical error. The footnote in the text was ¹¹, but the footnote should have been ¹.

The relationships among benzodiazepine dose, respiratory depression, and subsequent need for endotracheal intubation are poorly characterized, but higher doses of benzodiazepines may actually reduce the number of airway interventions. Our data are consistent with the finding that endotracheal intubation is more commonly a sequela of continued seizures than it is an adverse effect of sedation from benzodiazepines.¹¹ ^[1]

Here is some of the information from footnote ¹. One interesting aspect of this double-blind study is that there is a placebo group. Patients received 2 mg IV lorazepam, 5 mg IV diazepam (Valium), or IV placebo. Treatment could be repeated one time if seizures continued for more than 4 minutes or if seizures recurred.

Cardiorespiratory complications before arrival at the hospital and at the time of transfer were important secondary outcomes that relate to the safety of out-of-hospital therapy with intravenous benzodiazepines. Despite concern regarding the adverse effects of these agents, we found a trend toward lower rates of out-of-hospital complications (primarily respiratory compromise) in the active-treatment groups than in the placebo group. This suggests that respiratory complications associated with prolonged seizures may be more pronounced than those caused by intravenous lorazepam and diazepam given at relatively low doses.^[2]

The doses are low. The lorazepam dose is only half of the 4 mg used in the IV lorazepam vs. IM midazolam study.

The doses of midazolam and lorazepam used in this trial are consistent with the most effective doses for the treatment of status epilepticus that are reported in the literature.^9,10 Although these initial doses are higher than the ones used by many EMS systems and emergency physicians, they are the same as those approved for this indication and are in line with those used by epileptologists.^[1]

Is there added safety from the lower doses?

The epilepsy specialists and the FDA (Food and Drug Administration) do not recommend lower doses.

Were the low doses effective?

2 mg midazolam?

Does anyone really expect such a small dose to make a difference?

Despite the beneficial outcomes associated with intravenous lorazepam and diazepam, 41 to 57 percent of patients who received active treatment were still in status epilepticus at the time of arrival at the emergency department. These patients were more than twice as likely to require intensive medical care as those whose seizures ended outside the hospital. Differences in the causes of the episodes of status epilepticus are unlikely to account for this difference. These observations, coupled with the favorable risk–benefit profile associated with lorazepam and diazepam in this trial, suggest that higher doses should be studied to define the optimal therapy for patients with out-of-hospital status epilepticus.^[2]

An editorial refers to the study just published^[1] and to the benzodiazepine vs. placebo study.^[2] Describing the complications in the placebo study, the author wrote –

Successful termination was much more common in the two groups that received benzodiazepines (59% with lorazepam, 43% with diazepam, and 21% with placebo). Since respiratory distress was twice as common in the group given placebo as in either of the groups given a benzodiazepine, the best way to avoid the need for intubation is to stop seizure activity.^[3]

This presents an interesting conundrum. Doses of benzodiazepines (midazolam, lorazepam, diazepam, . . .) are often limited, due to a fear of causing respiratory complications.

When treating seizures, higher doses of benzodiazepines may actually protect patients from respiratory complications.

With a fatality rate around 10%, seizures are certainly not benign.

Maybe early treatment with high dose benzodiazepines can significantly decrease that fatality rate.

Finally, relatively few out-of-hospital interventions have been evaluated in randomized controlled trials,¹⁶ and when they have been evaluated carefully, therapies with intuitive appeal have often been found either to lack benefit or to cause harm to patients.^17-20 ^[2]

The irony is that we may be doing the opposite by limiting doses of benzodiazepines to less than what is recommended by the FDA.

What do you think?

See also Part I and Part II. To be continued in Part IV.

Footnotes:

Free Full Text from N Engl J Med. with link to PDF Download

^[3] Intramuscular versus intravenous benzodiazepines for prehospital treatment of status epilepticus.
Hirsch LJ.
N Engl J Med. 2012 Feb 16;366(7):659-60. No abstract available.
PMID: 22335744 [PubMed - in process]

Intramuscular Midazolam for Seizures – Part II

Rogue Medic — Sun, 19 Feb 2012 11:30:30 +0000

Also posted over at Rogue Medic (now at EMS Blogs).

While there have been studies comparing IM (IntraMuscular) midazolam (Versed) with IV (IntraVenous) anti-epileptic medications, this is a large study that compares IM midazolam with the best IV anti-epileptic medication in a double-blind, randomized, noninferiority trial.

All adults and those children with an estimated body weight of more than 40 kg received either 10 mg of intramuscular midazolam followed by intravenous placebo or intramuscular placebo followed by 4 mg of intravenous lorazepam.^[1]

For the study, there were two different doses for the auto-injector (similar to an EpiPen auto-injector). The doses were not small.

Midazolam for seizures is an off-label use both when given IM and when given IV.^[2]

The lorazepam IV doses in the study are according to the FDA label –

For the treatment of status epilepticus, the usual recommended dose of Lorazepam Injection is 4 mg given slowly (2 mg/min) for patients 18 years and older. If seizures cease, no additional Lorazepam Injection is required. If seizures continue or recur after a 10- to 15- minute observation period, an additional 4 mg intravenous dose may be slowly administered.^[3]

Unfortunately, my protocols only permit 1/4 or 1/2 the dose of lorazepam for seizures, which may be repeated every 5 minutes up to a maximum of one full dose recommended as the initial dose by the FDA.^[4] There is no adult IM use of midazolam.

There is often a concern about carefully adjusting pediatric doses. How did they handle that in this study?

In children with an estimated weight of 13 to 40 kg, the active treatment was 5 mg of intramuscular midazolam or 2 mg of intravenous lorazepam.^[1]

But such high doses will lead to deadly outcomes

Except that this excuse to give low doses is not supported by the authors of this study.

The relationships among benzodiazepine dose, respiratory depression, and subsequent need for endotracheal intubation are poorly characterized, but higher doses of benzodiazepines may actually reduce the number of airway interventions. Our data are consistent with the finding that endotracheal intubation is more commonly a sequela of continued seizures than it is an adverse effect of sedation from benzodiazepines.¹¹^[1]

That is a very interesting comment. The authors believe that intubations are increased by not controlling the seizure, rather than by giving large doses of a benzodiazepine. Unfortunately. I did not see anything to support that statement in the paper they cited as footnote 11.^[5]

See also Part I. To be continued in Part III, and Part IV.

Footnotes:

^[2] MIDAZOLAM HYDROCHLORIDE injection, solution
[Hospira, Inc.]
DailyMed
NLM
FDA label

I checked all of the injectable formulations of midazolam. They are the same. None include recommended dosing for seizures, but all include warnings about midazolam possibly causing seizures.

^[3] Lorazepam (lorazepam) Injection, Solution
[Baxter Healthcare Corporation]
DailyMed
NLM
FDA label

^[4] Seizure
Pennsylvania Statewide Advanced Life Support Protocols
7007 – ALS – Adult/Peds
Page 100/128
Free Full Text PDF of All ALS Protocols

Titrate until seizure stops.

Split the dose in half. Repeat the dose in 5 minutes.

There is no option for adult IM dosing.

^[5] A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children.
Chamberlain JM, Altieri MA, Futterman C, Young GM, Ochsenschlager DW, Waisman Y.
Pediatr Emerg Care. 1997 Apr;13(2):92-4.
PMID: 9127414 [PubMed - indexed for MEDLINE]