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ECG Case 2

10/23/2012 by Adam Thompson, EMT-P 1 Comment
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You respond to a residence for a 53 y/o female who fell unresponsive in her bathroom. As you arrive, you discover that she is in full cardiac arrest and you begin to attempt resuscitation. The patient is in v-fib and after two shocks, vas

opressin, Amiodarone, and one epinephrine bolus, she regains a pulse.You obtain a post-arrest 12-lead ECG. What is your interpretation of this ECG and what are some considerations for the care of this patient?

ECG Case 2 – Click to enlarge

Watch the full interpretation and case review below.


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ECG Case 1

10/20/2012 by Adam Thompson, EMT-P Leave a Comment
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You respond to a 70 y/o female with chest pain & dyspnea. Upon arrival you see that she is sitting upright with labored respirations, clinching her chest. She states that this has been getting worse all day, and it is currently 1700.

S - Chest Pain, dyspnea, and swelling

A – PCN & Sulfa

M – Lisinopril, Digoxin, Furosemide, Plavix, Omeprazole, Albuterol, and Singulair all on scene.

P – Patient’s dyspnea inhibits her from providing this info.

L – Cheeseburger for lunch at noon

E – Onset was after she woke up. She says she feels tired and doesn’t think she slept well.

Chest Pain:
O – Gradual
P – Laying down increases pressure
Q – Chest Pressure
R – Non-radiating
R – No relief
S – 6/10
T – Started this morning around 0700

The attached 12-lead was obtained. What assessment findings would you be interested in. What is your interpretation of the 12-lead ECG? Does this ECG fit with the patient presentation?

Paramedicine101: ECG Case 1

 


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My Favorite Resource For Medicine

06/12/2012 by brent Leave a Comment
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I wanted to share my favorite resource for medical information. By far the best resource I have found is the EMCrit blog. The author is Scott Weingart, an ED Intensivist from New York. I spend much of my time listening to the EMCrit Podcast, which is available free from iTunes. This is an amazing resource for both new and veteran medics. Lots of  new and up to date information. He is based in an Emergency Department so some of this information will not directly apply to Paramedicine but is still loaded with great information. Hope you take the time to check out this amazing resource. Located at EMCrit.org.

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Introducing a new contributor to Paramedicine 101

05/26/2012 by brent Leave a Comment
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My name is Brenton Birr. I was asked by Adam Thompson to contribute to the Paramedicine 101 blog. I currently work for Lee County EMS in Fort Myers, Florida and  have worked the past seven years at a level two trauma center.  I am here to bring some of that knowledge to the Paramedicine 101 blog. Through this blog I would also like to emphasize the more basic concepts of paramedicine that are many times overlooked by both new and veteran paramedics. Please bear with me as I am new to blogging, but will be adding my first informative post very soon.

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Does RSI Protect Against Aspiration of Stomach Contents

03/15/2012 by Rogue Medic 2 Comments
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Also posted over at Rogue Medic (now at EMS Blogs).

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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.

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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.

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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!

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Does this –

 


Image credit.

 

protect against this?

 


Image credit.

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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).

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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?

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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?

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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.

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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.

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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?

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Footnotes:

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[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.

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Filed Under: Airway Management, Heresy, Intubation, Pharmacology, Research, Rogue Medic

Intramuscular Midazolam for Seizures – Part VI

03/14/2012 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs).

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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)?

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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]

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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]

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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?

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

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Footnotes:

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[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]

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[2] MIDAZOLAM HYDROCHLORIDE injection, solution
[Hospira, Inc.]

DailyMed
FDA Label

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[3] ATIVAN (lorazepam) injection, solution
[Baxter Healthcare Corporation]

DailyMed
FDA Label

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[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]

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Filed Under: Heresy, Pharmacology, Research, Rogue Medic

Intramuscular Midazolam for Seizures – Part V

03/13/2012 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs).

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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?

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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?

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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.

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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.

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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.

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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.

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

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Footnotes:

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[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]

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[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

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Filed Under: Heresy, Pharmacology, Research, Rogue Medic

Intramuscular Midazolam for Seizures – Part IV

03/09/2012 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs).

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

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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]

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Click on images to make them larger.

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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.

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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.

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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.

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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.

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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.

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

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Footnotes:

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[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]

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Filed Under: Heresy, Pharmacology, Research, Rogue Medic

Nontraumatic out-of-hospital hypotension predicts inhospital mortality

03/07/2012 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs).

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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.

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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.

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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.

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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]

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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.

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

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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?

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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.

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Footnotes:

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[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]

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Filed Under: Assessment, Heresy, Research, Rogue Medic

Psychic vs. RAD-57

02/23/2012 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs).

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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.

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Image credits – 1, 2, and 3.

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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.

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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?

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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.

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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.

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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?

.

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