Paramedicine 101

WE ARE MOVING...

2010-09-10T17:56:00.000-04:00

Paramedicine 101 is joining up with EMSblogs.com.

We will be moving to www.Paramedicine101.com.

It is still a work in progress right now, but don't hesitate to head over to the new site, because that is where all the new posts will end up.

Thank you for your loyalty as a reader. I hope this doesn't inconvenience you at all.

- Adam Thompson, EMT-P

Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study – abstract

2010-09-07T17:27:00.003-04:00

I have moved Rogue Medic to EMS Blogs. Also posted over at Rogue Medic and at Research Blogging.

Go check out the rest of what is available at EMS Blogs and at Research Blogging.

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Over at 510 Medic, there is an interesting abstract of a new article on treatment of tension pneumothorax. Frequency of Inadequate Needle Decompression in the Prehospital Setting.

CONCLUSIONS: In this study, 26% of patients who received needle thoracostomy in the prehospital setting for a suspected PTX appeared not to have had a PTX originally, nor had 1 induced by the needle thoracostomy. It may be prudent to evaluate such patients with bedside ultrasound instead of automatically converting all needle thoracostomies to tube thoracostomies.^[1]

I have not read the full text. ~~I do not have access to this journal. If anyone can send me the full text, I would like to address some of the details, rather than just speculate about them.~~ Late entry - I have received the article. Thank you to Jeff Williams and Jeremy Blanchard. I will write more about the full text later on.

510 Medic makes some important points and asks some good questions. Then 510 Medic asks -

So if we subscribe to the goal of “first do no harm” and those 15 patients didn’t have a pneumothorax induced by the procedure, is their discomfort worth proper treatment for the remaining 42 patients?^[2]

I think that there is a more important question.

Should we assume that the presence of a pneumothorax is an indication for needle decompression?

A pneumothorax is not the same as a tension pneumothorax. Even the definition of a tension pneumothorax is not easy to agree on. I tend to treat with opioids what many others would treat with needle decompression. I have not had any of these patients deteriorate, while in my care. They received chest tubes in the trauma center.

Should we assume that the presence of a pneumothorax is an indication for needle decompression?

57 patients with a prehospital diagnosis of tension pneumothorax. Yes, EMS does diagnose, but that is a discussion for elsewhere. Yes, these patients were diagnosed by EMS with tension pneumothorax, unless we are suspecting acupuncture, because what other prehospital indication is there for sticking a needle into a patient's chest?

Out of 57 patients diagnosed with tension pneumothorax, only 42 patients had a pneumothorax.

How many patients had a tension pneumothorax at the time the needle was stuck into the chest wall?

How many of those patients would have been better off if treated with something other than a needle?

How many complications were there from the needle decompression?

Am I wrong to use italics to highlight the word decompression, since so many of the patients did not have anything to decompress?

We rush to perform procedures that we have little experience with. Isn't this a situation likely to lead to misdiagnosis?

Isn't the infrequent use of needle decompression for suspected tension pneumothorax likely to lead to operator error?

The actual occurrence of tension pneumothorax appears to be much less frequent than the prehospital diagnosis of tension pneumothorax. Isn't that an indication of a failure to properly educate medics?

Footnotes:

^[1] Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study.
Blaivas M.
J Ultrasound Med. 2010 Sep;29(9):1285-9.
PMID: 20733183 [PubMed - in process]

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^[2] Frequency of Inadequate Needle Decompression in the Prehospital Setting
510 Medic
Article

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Research: Prehospital Pain Management

2010-09-06T21:18:00.001-04:00

Check this out...

I'm not sure why IV Fentanyl wasn't compared to Morphine, but the study is interesting none-the-less.

Prehosp Emerg Care. 2010 Oct-Dec;14(4):439-47. [Pubmed]
Effectiveness of morphine, fentanyl, and methoxyflurane in the prehospital setting.
Middleton PM, Simpson PM, Sinclair G, Dobbins TA, Math B, Bendall JC.

Abstract

Abstract Objective. To compare the effectiveness of intravenous (IV) morphine, intranasal (IN) fentanyl, and inhaled methoxyflurane when administered by paramedics to patients with moderate to severe pain. Methods. We conducted a retrospective comparative study of adult patients with moderate to severe pain treated by paramedics from the Ambulance Service of New South Wales who received IV morphine, IN fentanyl, or inhaled methoxyflurane either alone or in combination between January 1, 2004, and November 30, 2006. We used multivariate logistic regression to analyze data extracted from a clinical database containing routinely entered information from patient health care records. The primary outcome measure was effective analgesia, defined as a reduction in pain severity of >/=30% of initial pain score using an 11-point verbal numeric rating scale (VNRS-11). Results. The study population comprised 52,046 patients aged between 16 and 100 years with VNRS-11 scores of >/=5. All analgesic agents were effective in the majority of patients (81.8%, 80.0%, and 59.1% for morphine, fentanyl, and methoxyflurane, respectively). There was very strong evidence that methoxyflurane was inferior to both morphine and fentanyl (p < 0.0001). There was strong evidence that morphine was more effective than fentanyl (p = 0.002). There was no evidence that combination analgesia was better than either fentanyl or morphine alone. Conclusion. Inhaled methoxyflurane, IN fentanyl, and IV morphine are all effective analgesic agents in the out-of-hospital setting. Morphine and fentanyl are significantly more effective analgesic agents than methoxyflurane. Morphine appears to be more effective than IN fentanyl; however, the benefit of IV morphine may be offset to some degree by the ability to administer IN fentanyl without the need for IV access.

Pain management is one of those things commonly under done by paramedics. I believe common reasons for this lack of treatment include laziness, apathy, and disbelief. Paramedics don't want to do the added paperwork that goes with administering a controlled substance. They may not care too much about the pain that their patient is in, and are much more concerned about life-threatening conditions. Finally, the existence of drug seekers most-definitely decreases the amount of pain meds administered prehospitally. Whatever the reason, it isn't a good one. If your patient complains of pain, it should be treated. An ice pack or positioning may be enough for some, while heavy doses of potent narcotics may be required for others. We have the tools, now lets use them.

I have added the Wong-Baker 'faces' pain scale here to remind you of how to judge your pediatric patient's pain. The old one through ten severity scale is suffice for adults.

Learn It: Angioedema

2010-09-05T13:54:00.000-04:00

Angioedema

Sometimes referred to as Quinke's Edema, angioedema is that swelling we see that is most apparent around the mucosal areas of the face. Consider Hives as swelling on the surface of the skin, and angioedema as swelling beneath the skin.

The most common cause of this type of swelling without the presence of Hives is hypersensitivity to ACE inhibitors.

ACE = Angiotensin converting enzyme. This converts angiotensin one into angiotensin two.

ACE inhibitors block ACE.

Bradykinin is a peptide that has a role with all forms of angioedema. It is a potent vasodilator that increases permeability and allows the accumulation of fluid within the interstitial space.

ACE is one of the main ways that bradykinin is degraded. So when we inhibit the production of ACE, we are then inhibiting the degradation of bradykinin. We then have this run away peptide and subsequent swelling.

Many patients that suddenly present with severe angioedema have been taking ACE inhibitors, such as lisinopril, for a long period of time. They may have never had any issues before, but out of no where have this severe reaction. This type of reaction is most common in the African-American population, but may occur in anyone.

There are other types of angioedema, including the traditional allergic reaction. Those are more well known and prepared for.

Treatment

As you can see from the pictures above, swelling may be within the oropharynx. This can cause an airway obstruction, and aggressive airway management should be advocated.

This patients may be obtunded and snoring as you enter the scene. They have been confused for diabetics, or acute coronary syndrome patients due to their initial impression.

It is common for these patients to undergo cricothyrotomy due to complete glottic obstruction. Moving quickly is imperative to prevent severe hypoxia and cardiorespiratory arrest.

The usual drugs used for anaphylactic reactions are indicated.

- Epinephrine to reduce the vasodilation.

- Crticosteroids & antihistamines.

So the next time you run on a patient that is presenting with swelling in the absence of hives, think angioedema, and act fast!

Fire & EMS Blogger Warning: Righthaven Lawsuits

2010-08-31T10:23:00.002-04:00

Also posted at Star of Life Law.

Fellow Fire and EMS bloggers, if you have not heard of Righthaven, LLC, you might be soon. In the name of a federal copyright lawsuit. Here is what you need to know:

1. Righthaven, LLC is a Las Vegas company established to sue bloggers who clip news content. Most newspapers firmly request bloggers or aggregators take down infringing content and link back to the paper. By comparison, Righthaven goes directly to suing, without any request to take down.

2. Righthaven has issued more than 100 lawsuits since its inception. See Righthaven Victims. See also Righthaven Lawsuits.

3. Righthaven's first client was Nevada-based Stephens Media. The Las Vegas Review Journal is Stephens’ flagship.

4. Righthaven has just struck a deal with Arkansas-based WEHCO Media to expand its copyright litigation campaign, in which bloggers and aggregators across the country are being sued on allegations of infringement. WEHCO controls 28 papers, including the Arkansas Democrat-Gazette in Little Rock, and 13 cable stations largely in the south.

5. Go here for a complete list of Righthaven-owned domains and newspapers.

6. Go here for a Firefox add-on that will prevent you from accessing Righthaven-owned content.

7. From Clayton Cramer, The Armed Citizen, a Righthaven lawsuit victim:

"For those who think that this could be settled out of court cheaply: think again. Other defendants who have approached Righthaven without a lawyer to settle this matter have been told variously, "$7500" or "low five figures" for a single newspaper article infringement."

8. Here is some guidance on how to properly cite news articles on your blog. Post the headline of the story and then the first paragraph with a link to the original story. Like this:

Jogger was listening to iPod when plane hit him, coroner says
The (Hilton Head) Island Packet
Tuesday, Mar. 16, 2010

A Georgia man was running and listening to his iPod on the beach on Hilton Head Island when he was killed by an airplane that made an emergency landing Monday near Palmetto Dunes, the Beaufort County Coroner's Office said today.

The rest of the article can be viewed by clicking here.

Hat tip to Ryan Giles.

9. Police your site. Remove or update potentially infringing posts. Properly cite and link to news sources.

10. If you are a Fire/EMS blogger and get served with a Righthaven lawsuit, feel free to email me.

Drug Shortages Affect Those Still in the Dark Ages – Furosemide

2010-08-26T20:24:00.007-04:00

I have moved Rogue Medic to EMS Blogs. Also posted over at Rogue Medic and at Research Blogging.

Go check out the rest of what is available at EMS Blogs and at Research Blogging.

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In the current JEMS, there is an embarrassing article. Drug Shortage Possible in N.Y.

It seems that the drugs that people are worried about are lidocaine, furosemide, 50% dextrose, and epinephrine 1:10,000 preloaded syringes. Here, I will discuss furosemide.

Furosemide is not appropriate for EMS patients, because there are more appropriate drugs, more appropriate other treatments, and it is too often given to patients who have pneumonia.

MANAGEMENT OF APE
Fluid accumulation in the lungs associated with APE, until recently, was attributed to excess accumulation of total body fluid. Accordingly, treatment of APE was aimed at removing excess fluid from the lungs by promoting massive diuresis. However, this explanation for APE could not reconcile the fact that APE typically occurs during early morning hours when fluid intake is minimal. The current explanation is that APE results from fluid redistribution within the body whereby a part of the intravascular volume is redistributed to the lungs as a consequence of increased intravascular pressure as outlined above.¹³ Primary objectives for the treatment of acute CHF are to reduce pulmonary capillary pressure, to redistribute pulmonary fluid, and to improve forward flow.^12,13 These may be achieved by reducing LV preload and afterload, providing ventilatory and inotropic supports, and identifying and treating the underlying etiology of the syndrome (Table 3). It should be recognized that these treatment measures are intended for APE patients who are normotensive or hypertensive and not those who are hypotensive. The latter comprises cardiogenic shock secondary to severe LV systolic dysfunction; treatment of these critically ill patients is beyond the scope of this review.^[1]

That is a big paragraph, but there is a lot of information in there. Enough to convince us that we should not be using furosemide to treat an acute onset/exacerbation of heart failure.

In the chart below, before furosemide in treatment there are plenty of other treatments. Notice that only oxygen comes before NTG (NiTroGlycerine) and the more severe the symptoms, the more NTG is given.

Mild symptoms - One 0.4 mg NTG spray/tab - repeated every 4 to 5 minutes.

Moderate symptoms - High-dose NTG, which is explained below.

Severe symptoms - Two to five 0.4 mg sprays/tabs at a time - repeated every 3 to 5 minutes.

But, but, but, but, but, . . . . . we can only give a maximum of 3 NTG - ever.

Then you need to get a better medical director, because your medical director has you killing patients.

Am I being too subtle?

Another treatment that is very effective is CPAP (Continuous Positive Airway Pressure) which is a BLS (Basic Life Support) skill, except where medical directors like to kill patients. When using CPAP (a form of NIPPV - Non-Invasive Positive Pressure Ventilation), NTG paste can be applied. Do not be shy with the paste, because nothing is absorbed well through the skin when the skin is pale. Pale means a lack of circulation. Also, since the appropriate dose is much more than standard NTG dosing, there is not much reason to hold back.

I disagree about the placement of CPAP at the bottom. CPAP should be started right away. This was published in 2003, so it is kind of old and conservative.

You call that NTG use conservative?!?!?

I do. I have given dozens of NTG in a period of 10 to 20 minutes and never had a patient experience any adverse effects while in my care or at the hospital. I have written elsewhere about the superstitious way we approach NTG.

Furosemide is in there, but only if the patient has peripheral edema. If there is no peripheral edema, is fluid overload the problem? That is a fluid redistribution problem. There is fluid in the wrong place, but that does not mean that the whole body is overloaded with fluid or that putting a bunch of fluid in the bladder is going to make things better. Moving fluid to the bladder does not mean that we are removing it from the lungs any more than we are removing fluid from anywhere else.

Click on the chart to make it bigger. I know I can't read any of it at this size. This is from the same paper as the paragraph above.

Well, that is just one paper. Nobody else would be so irresponsible as to recommend such large doses of NTG.

Then let's read about what they do in the ED (Emergency Department).

Most patients who experience CPE, however, do not have ECG evidence of an acute dysrhythmia or AMI. Treatment should therefore be aimed at redistributing the excessive pulmonary interstitial ﬂuid into the systemic circulation, which improves alveolar oxygen-carbon dioxide exchange and hypoxia; therefore, pharmacologic agents that provide preload reduction and afterload reduction should be administered. In some cases, inotropic support is required also.^[2]

What drugs do we use to provide preload reduction and afterload reduction?

Nitroglycerin
The most eﬀective and rapidly-acting preload-reducing medication is nitroglycerin (NTG) ^[21–25]. Multiple studies have demonstrated the superiority of NTG over furosemide ^{[21,24,26–28]} and morphine sulfate ^[28–30] for preload reduction, symptomatic improvement, and safety. NTG can be administered in sublingual, IV, or transdermal form, although the transdermal absorption can be erratic in the patient in extremis. NTG also has the beneﬁt of a short half-life; therefore, if the patient develops a precipitous fall in blood pressure (generally uncommon in CPE {Cardiogenic Pulmonary Edema} patients), the blood pressure should return to previous values within 5 to 10 minutes of discontinuation of administration.^[2]

But what about the dose?

In one study ^[26], 3 mg IV boluses of NTG were administered every 5 minutes to patients who had developed CPE, a dose equivalent to a 600 mg/min infusion. This protocol was found to be safe, well-tolerated, and eﬀective for these patients and associated with reduced need for mechanical ventilation and more rapid resolution of symptoms. Standard anti-anginal dosages of sublingual NTG with which most physicians are comfortable (ie, 400 µg every 5 minutes), has the bioequivalence of an IV NTG infusion of 60 to 80 µg/min. Physicians should, therefore, be comfortable with the safety of even higher dosages of NTG for patients who experience CPE and usually present in a hyper-adrenergic state with moderately-to-severely elevated blood pressures.^[2]

That is 7 1/2 times to 10 times the standard dose of NTG - with no problems.

Maybe that maximum of 3 NTG is something that should be ignored. The AHA (American Heart Association) seems to be ignoring it. Just try to find a limit on NTG administration in the current ACLS, which is from 2005.

These papers are available in PDF format, so you can print them out and hand them to your medical director and/or to the other doctors in the ED.

These are important papers. Both are review articles. One is written for EMS, while the other is written for the ED.

If you are feeling aggressive, maybe you can write on the bottom, Call me about improving the protocols we use to treat our patients.

There is one problem with this. This will lead to fewer intubations.

The best intubation is the intubation that is prevented by excellent patient care.

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Footnotes:

^[1] Prehospital therapy for acute congestive heart failure: state of the art.
Mosesso VN Jr, Dunford J, Blackwell T, Griswell JK.
Prehosp Emerg Care. 2003 Jan-Mar;7(1):13-23. Review.
PMID: 12540139 [PubMed - indexed for MEDLINE]

Free Full Text PDF

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^[2] Modern management of cardiogenic pulmonary edema.
Mattu A, Martinez JP, Kelly BS.
Emerg Med Clin North Am. 2005 Nov;23(4):1105-25. Review.
PMID: 16199340 [PubMed - indexed for MEDLINE]

Free Full Text PDF

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EMS Educast Episode 67

2010-08-26T19:11:00.000-04:00

Greg Friese from EMS Educast invited me to guest cohost on episode 67. On the show was David Page from the St. Paul EMS Academy.

Make sure to go check it out.

Thanks for stopping by,

Adam Thompson, EMT-P

Drug Shortages Affect Those Still in the Dark Ages – Lidocaine

2010-08-24T18:06:00.006-04:00

I have moved Rogue Medic to EMS Blogs. Also posted over at Rogue Medic and at Research Blogging.

Go check out the rest of what is available at EMS Blogs and at Research Blogging.

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In the current JEMS, there is an embarrassing article. Drug Shortage Possible in N.Y.

It seems that the drugs that people are worried about are lidocaine, furosemide, 50% dextrose, and epinephrine 1:10,000 preloaded syringes. Here, I will discuss lidocaine.

Lidocaine is not appropriate for EMS patients, because there are more appropriate drugs. Lidocaine is still used for cardiac arrest, even though there is absolutely no reason to believe that it does anything positive for the patient.

There is no evidence that any antiarrhythmic drug given routinely during human cardiac arrest increases survival to hospital discharge. Amiodarone, however, has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine.^[1]

In other words, amiodarone doesn't work, but lidocaine is even worse.

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Lidocaine is also used for ventricular tachycardia with similar lack of effect.

Lidocaine terminated ventricular tachycardia in four of 31 patients, ajmaline in 19 of 30 patients (P<0.001).^[2]

Lidocaine is no better than holding the patients hand or any other placebo. Spontaneous remission of ventricular tachycardia should occur in more than 4 out of 31 patients.

DC shock was used in 16 nonresponders (22.9%) to procainamide and 10 non-responders (50%) to lidocaine.^[3]

Only 35% of patients improved after lidocaine. Maybe they improved because of lidocaine - maybe not. More important is that 50% of patients who received lidocaine ended up being cardioverted. Did they require cardioversion because of the lidocaine?

Would you recommend a drug that leads to half of patients being cardioverted?

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Footnotes:

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^[1] Medications for Arrest Rhythms
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Free Full Text

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^[2] Electrophysiological and haemodynamic effects of lidocaine and ajmaline in the management of sustained ventricular tachycardia.
Manz M, Mletzko R, Jung W, Lüderitz B.
Eur Heart J. 1992 Aug;13(8):1123-8.
PMID: 1505562 [PubMed - indexed for MEDLINE]

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^[3] Efficacy of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia.
Komura S, Chinushi M, Furushima H, Hosaka Y, Izumi D, Iijima K, Watanabe H, Yagihara N, Aizawa Y.
Circ J. 2010;74(5):864-9. Epub 2010 Mar 26.
PMID: 20339190 [PubMed - indexed for MEDLINE]

Free Full Text PDF

Table 3 is from this paper. As you can see, lidocaine is a joke compared to procainamide.

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Church of the Blog O Sphere: EMS Garage Episode 99

2010-08-17T12:32:00.016-04:00

Also posted over at Rogue Medic. I have moved to EMS Blogs. Go check out the rest of what is there.

On the most recent EMS Garage - Church of the Blog O Sphere: EMS Garage Episode 99, we spent a bit of time discussing how to persuade people that we should change things and how we can determine what is the truth.

Listen to the show.

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Need Your Help

2010-08-15T16:45:00.000-04:00

I am looking for help with the following projects:

Paramedicine 101 Podcast
Interactive Educational Software

I am looking for sponsors for the Podcast. Please contact me at Paramedicine101@gmail.com for pricing and advertising options.

I am also looking for software developers to assist me with the creation of something I have been working on. It would be an interactive presentation/educational program. Assistance with this would gain you commission on any income made.

Last but not least. I am looking for an artist/illustrator. Someone, preferably with experience illustrating the human anatomy.

Contact Adam Thompson at Paramedicine101@gmail.com

McLearning and 12-Lead ECG interpretation

2010-08-15T12:16:00.001-04:00

I've been giving a lot of thought lately to paramedic education and the problem of 12-lead ECG interpretation.

Specifically, the reasons why paramedics aren't taught to actually read a 12-lead ECG and are instead given a crash course in "STEMI recognition" which does not prepare the student to differentiate between the ST-elevation of acute STEMI and other causes of ST-elevation.

This TED Talk by Dan Meyer about high school math education struck a chord with me. I highly recommend the entire talk, but the most relevant part for this discussion starts at 01:50.

Here's the part that really resonated with me:

"David Milch, creator of Deadwood and other amazing TV shows [...] swore off creating contemporary drama -- shows set in the present day -- because he saw that when people filled their minds with 4 hours a day of, for example, 2 1/2 Men, it shapes the neuro-pathways in such a way that they expect simple problems. He called it an "impatience with irresolution". You're impatient with things that don't resolve quickly. You expect sitcom-sized problems that wrap up in 22 minutes, 3 commercial breaks and a laugh track.

I'll put it to all of you -- what you already know. No problem worth solving is that simple."

Doesn't that exactly describe the paramedic approach to 12-lead ECG interpretation?

EKGs for Dummies, 12-Leads Made Easy, Rapid STEMI ID, etc. etc. etc.

Just the "need to know" information without all the difficulty of axis determination, bundle branch blocks, electrolyte derangements, differential diagnosis of tachycardias, primary and secondary ST-T wave abnormalities, identifying acute STEMI in the presence of STE-mimics, and other things that we have no patience for because we can't learn it in 22 minutes.

As if we can jump straight to the finish line and enjoy the fruits of victory without ever preparing for the race.

The problem is compounded by policy makers who "don't know what they don't know" (thank you Don Rumsfeld). They consider it a foregone conclusion that comprehensive 12-lead ECG knowledge is not practical for paramedics.

I say that it's indispensable.

Show Me Your Rig

2010-08-14T10:28:00.001-04:00

On the Paramedicine 101 Facebook page, I am asking the readers to show off their ambulance. Maybe we can get to know each other a little by gawking at the trucks we drive. Go post a picture of your chariot.

Research: Management of the Airway in the Trauma Patient

2010-08-13T17:55:00.000-04:00

Check this out...

J Trauma. 2010 Aug;69(2):294-301. [Pubmed]
Prehospital airway and ventilation management: a trauma score and injury severity score-based analysis.
Davis DP, Peay J, Sise MJ, Kennedy F, Simon F, Tominaga G, Steele J, Coimbra R.

Abstract

BACKGROUND:: Emergent endotracheal intubation (ETI) is considered the standard of care for patients with severe traumatic brain injury (TBI). However, recent evidence suggests that the procedure may be associated with increased mortality, possibly reflecting inadequate training, suboptimal patient selection, or inappropriate ventilation. OBJECTIVE:: To explore prehospital ETI in patients with severe TBI using a novel application of Trauma Score and Injury Severity Score methodology. METHODS:: Patients with moderate-to-severe TBI (head Abbreviated Injury Scale score 3+) were identified from our county trauma registry. Demographic information, pre-resuscitation vital signs, and injury severity scores were used to calculate a probability of survival for each patient. The relationship between outcome and prehospital ETI, provider type (air vs. ground), and ventilation status were explored using observed survival-predicted survival and the ratio of unexpected survivors/deaths. RESULTS:: A total of 11,000 patients were identified with complete data for this analysis. Observed and predicted survivals were similar for both intubated and nonintubated patients. The ratio of unexpected survivors/deaths increased and observed survival exceeded predicted survival for intubated patients with lower predicted survival values. Both intubated and nonintubated patients transported by air medical crews had better outcomes than those transported by ground. Both hypo- and hypercapnia were associated with worse outcomes in intubated but not in nonintubated patients. CONCLUSIONS:: Prehospital intubation seems to improve outcomes in more critically injured TBI patients. Air medical outcomes are better than predicted for both intubated and nonintubated TBI patients. Iatrogenic hyper- and hypoventilations are associated with worse outcomes.

This publication is prestigious enough to trust the validity of the study. It looks as if enough patients were ruled-in to take consideration of the evidence. With the increase in ICP (intracranial pressure) that intubation causes, it has been theorized in the past, that intubating the TBI patient only made them worse. However, this study shines a different light. So what do you think? The discussion is open.

I am not a cretin

2010-08-12T08:06:00.005-04:00

Back during EMS Week, EMS1.com held a writing contest. Kelly Grayson, AKA Ambulance Driver called on us EMS bloggers to make submissions. The theme was Anytime, Anywhere, We'll be there. I am not sure who one, but the top 6 can be seen here. Below is my submission. Enjoy...

I am not a cretin

I am but a mere individual amongst a whole world of professionals. I am a thrill seeker, but not the kind that jumps off cliffs with a self-packed parachute attached to his back. I am educated in my craft, and I do it well. Many, even with my hard earned five years of experience, could still consider me a rookie. I am an educator, but not a professor. An expert, but not a scientist. A manager, but I lack a work force. I'm not an athlete, actor, or politician, but I believe I make a difference. I am a paramedic.

As a paramedic, we make many promises. Some are simply shrugged off or overlooked. "I promise I will take care of your father to the best of my abilities", or "I promise, just one little poke". Some of these promises are ever so important, but understood without ever having the need for verbal explanation. Anytime, anywhere, we'll be there. Now that's a promise.

911, the one phone number that you can call and pretty much expect an answer on the other end every time — excluding a few flukes. Jimmy Noolan was hoping that was the case when he dialed that number from a payphone outside of a 7-eleven. You see, Jimmy doesn't get too many voices talking back to him on the other end of calls he often makes. His wife and son tragically left him prior to him being ready to let them go, as if he could ever be ready for that. He chose to drown his pain with his buddy Jack, and built a pretty strong relationship with ‘ole Jack. His drinking problem weighed heavy on his life, and what remaining family members he had, simply gave up on him. Out of a job, family, and home, Jimmy like so many, took to the streets.

A man who seemingly cared so little about his own life had called 911. But this isn't the first time. Jimmy happens to be, what I call a repeat offender. He calls often, usually with the chief complaint of loneliness, hunger, or cold and wet syndrome. Thought by many as a burden to our already busy EMS system, and unfortunately treated as such all too often.

The tones drop back at the station and the call comes in, Medic 7, respond to the 7-11 for a possible heart attack. My partner and I look at each other with grins and scowls due to the premature diagnosis made by our illustrious dispatcher. We know it isn't the dispatcher's fault, but give us the symptoms, and let us tell you what it is. We also throw the possibility back and forth of this just being another transient at a payphone — of course keeping the worst possible case scenario in the back of our heads. This is a training truck, and we have enjoyed the three-person crew all day, running these calls smoother than our freshly shaved faces.

We don't kill ourselves getting there, taking the lights and sirens response easy. If anything, it will give the local fire guys time to practice their BLS skills. We already had our dinner in us, and there was no rush to get this over with. As we pull up, the red truck with the flashing lights gave us a good idea where the patient was located. A group of well-trained, firefighters were huddled around what looked to be a patient. A familiar face was finally visible as we approached, and I could hear my partner whisper "oh gosh, it's Jimmy". Yep, there he was in his usual getup, a tattered dirt-stained blue flannel and similarly filthy ripped jeans with his sock-less feet in a pair of unlaced brown construction boots.

The firefighters gave me the typical report: "O2, aspirin, and vital signs, he wants to go downtown." Going downtown was fine with me, it was right around the corner from the station, and they were use to Jimmy by now. Sure, it isn't a cardiac facility, but this was Jimmy, not a real patient — right?

We packaged Jimmy on the stretcher, and wheeled him to the truck. My partner hollered up front to our EMT, "downtown, kill the lights". Something happened at this very moment, something I had heard of, but never experienced. My gut was disagreeing with my lackluster treatment. Another glimpse at Jimmy told me something was wrong. He was seemingly pretty sober. He was not his normal sad, and lonely self. He was scared, and from the looks of his pale, damp skin, he was sick too! I gave my partner a look only understood by fellow EMS-ers. He asked what was wrong, and I replied, "Just let me get the 12-lead done before we start heading that way".

Sure enough, Jimmy was having an anteroseptal myocardial infarction — or a heart attack represented by ST-elevation in leads V1 thru V4. Looks like the dispatcher was right. The face on my partner when I showed him the ECG was indescribable. Pucker factor had now set in due to us being behind the ball. Humbled, a new gear was locked in, and our treatment strategy quickly changed. Obviously, so did our destination. STEMI center, here we come, only thirty some-odd minutes to go.

On the way to the hospital, new modalities were added to Jimmy's usual treatment of choice — compassion. Jimmy went into a short-lived lethal arrhythmia during the ride. Luckily Jimmy had the paramedics that he called for, not those guys that were about to take him downtown. He was quickly stabilized with our new sense of preparedness. We activated the cath-lab to facilitate quicker treatment on the way. Had two IV lines in him, some nitroglycerine, and a little morphine.

I held Jimmy's hand and told him he was going to be okay. Something I had told him so many times before, only this time I think I was listening to my words more than he was.

Jimmy had a massive occlusion to one of his coronary arteries. He underwent cardiac angiography and recovered well. It was a longer road than usual to the cardiac hospital that night. I thank God for that moment of realization, without it; his lifesaving treatment would have been delayed. I haven't seen or heard about Jimmy since, but I am sure he is still around, and you better believe that the next time he calls — anytime, anywhere, we'll be there. Only this time, without any preconceived notions — because I am a paramedic.

Names and events have been altered to protect the patient's privacy.

ECG: 40 y/o Female with Chest Pain

2010-08-11T22:49:00.000-04:00

Also Posted over at ECG Experts

Submission thanks to Tim Waters, CCEMTP of Lee County Medstar

40 yo female, thin build with no history/meds/allergies. + smoker. Works as painter outside and was painting when developed pain in her upper chest/left arm which is the same she uses to paint. Also adds that she has been moving and lifting numerous heavy objects over the past week and since then has been having these episodes of shoulder discomfort. Pain is non-radiating with moderate reproducibility with movement and inspiration. I forget what severity scale she gave it but was definitely uncomfortable. Onset was about 3 ½ hours prior to presentation while painting with her trying to work through the pain until it became to unbearable.. Denies nausea, is diaphoretic but has been working outside.

#CoEMS: CPR Effectiveness

2010-08-11T18:29:00.002-04:00

Chronicles of EMS, A Seat at the Table takes on CPR effectiveness. The Las Vegas video that they mention can be found below as well. Keep up the good work Justin and Mark!

Side note - ILCOR, The International Liaison Committee On Resuscitation has not found any supporting evidence for the Autopulse. They are the ones whom do the research for AHA. Also, transporting patients without a pulse should be re-looked at by any agency performing this practice. The initial treatment at the ER will not differ from the treatment we provide at the scene per ACLS guidelines. Why not give the patient the best chance possible. If they don't get a pulse back on scene, it is probably never going to come back--that's just the facts.

Man vs. Machine

Product Review: AHA's Rapid STEMI ID

2010-08-11T11:07:00.001-04:00

I was asked a few months ago to review the American Heart Association's STEMI recognition educational software. This software was created in response to a deficit found during Mission:Lifeline.

Here is the review I gave word for word:

Link to Learn: Rapid STEMI ID

First, I would like to say that it is not advocated to teach 12-lead ECGs in a STEMI vs. not a STEMI manor. While the intentions seem good, there is much more to learn regarding 12-lead ECG interpretation that this type of course does not cover. There is an overwhelming need for a more comprehensive resource for prehospital care providers, and other emergency medical personnel, for that matter.

It is my belief that the ACLS course should provide the base of 12-lead ECG knowledge while an online course could be adequate for continuing education. Initial training could include the six-step method of ECG interpretation.

Six-Step Method:

Rate & Rhythm
Axis determination
Complex, wave, and segment durations
Morphology
STE-Mimics
Ischemia, Injury, Infarct

This method could be taught extensively while breaking down each part to include the physiology of abnormalities. The Learn: Rapid STEMI ID course is a good start, but is at an educational level below that of what prehospital care providers should be at. It is also not adequate enough to be part of the curriculum within a paramedic program. I don’t feel an initial education in 12-lead ECG interpretation should be from an online course because of the inability to ask questions.

Learn: Rapid STEMI ID

Pros:

- The interactive software is top notch.

- The graphics used for the cardiology portion are very nice

- For the most part the cardiology review is very factual

- There is a good amount of ECG cases

- The cost seems to be about right for this type of course

Cons:

- This course is designed only for STEMI recognition, not 12-lead interpretation. While an important part of 12-lead interpretation, it is not the only ailment that can be determined.

- With the absence of any presentation outside of STEMI comes the lack of education regarding axis shift, rate changes, pacemaker changes, bundle branch blocks, electrolyte imbalances, etc. It is possible to create this course in conjunction with more comprehensive resources. For example, using the six-step method, this course would include steps five and six.

- The cardiology review is good, but it should also be explained that some patients have slight differences in their coronary arteries (i.e. stenosis, dominant RCA, dominant Cx).

- During the explanation of electrode application, there should be information about commonly misplaced electrodes and the need to remove all clothing on the patient from the waste up.

- There is no list of indications for 12-lead ECG interpretation. While there is a good explanation of typical and atypical ACS symptoms, ACS symptoms are not the lone reason to acquire a 12-lead ECG. Some research has shown that paramedics have not performed ECGs on nearly half of patients that present with STEMI at emergency departments.

- No information was provided about UA/NSTEMI, informing the learner that it is possible that the patient is suffering from an AMI in the absence of ST-Elevation.

- It is explained how to identify ST-Elevation, Q-waves, and Hyperacute T-waves, but there is no explanation of the physiology. A better understanding of the reasoning behind pathological changes will improve the overall efficiency of 12-lead ECG interpretation.

- There should be more information regarding posterior wall MI changes (i.e. reciprocal changes in septal leads, R/S ratio >1).

- One very easy way to determine the J-point’s location is to identify the J-point in a lead above or below the lead in question.

- Upward concavity is not a conclusive finding with early repolarization. While the “smiley face method” is a good way to get an idea of the ST morphology, it is not the only way to differentiate early repolarization from STEMI. Notched J-points, and mean R-wave amplitude in V2-V4 greater than 5 mm are both indicative of benign early repolarization.

- The information on the STE-Mimics that where covered was good. However, there is a lot more that could be provided.

o LVH was covered, but not RVH

o Pericarditis symptomology is the easiest way to differentiate it from STEMI.

o Hyperkalemia vs. Hyperactute T-waves

o Bundle branch blocks

o Brugada Syndrome

- Contiguous leads should have been explained better V1 & V6 are not contiguous.

- The differentiation between Septal, Anterior, and Low Lateral should be made. V1-V6 are not all considered anterior.

- The depth of Q-waves was not covered pathological vs. physiological. Width was appropriately taught, but not depth.

- It should be made known that MI is not the most common cause of ST-Elevation.

Overall, I am pleased to see that the AHA is making an attempt at 12-lead ECG education. I am a big fan of the AHA and its use of evidence-based medicine. In fact, there is plenty of evidence supporting ECG findings, and a need for better interpretation. Here is an example of something that might be missed out on if this course was the base of the responding paramedic’s ECG knowledge; patient with syncope who has long QT syndrome or Brugada syndrome. This patient may never even have a 12-lead ECG obtained even though that the two conditions described can both be lethal. I am optimistic about the possibilities to come.

Research: Management of the Airway in the Burn Patient

2010-08-10T10:44:00.000-04:00

Check this out...

J Burn Care Res. 2010 Jul 14. [Epub ahead of print]
Pre-Burn Center Management of the Burned Airway: Do We Know Enough?
Eastman AL, Arnoldo BA, Hunt JL, Purdue GF.

Abstract

Despite the traditional teaching of early and aggressive airway management in thermally injured patients, paramedics and medical providers outside of burn centers receive little formal training in this difficult skill set. However, the initial airway management of these patients is often performed by these preburn center providers (PBCPs). The purpose of this study was to evaluate the authors' experience with patients intubated by PBCPs and subsequently managed at the authors' center. A retrospective review of a level I burn center database was undertaken. All records of patients arriving intubated were reviewed. From January 1982 to June 2005, 11,143 patients were admitted to the regional burn center; 11.4% (n = 1,272) were intubated before arrival. In this group, mean age was 37.1 years, mean burn size was 35.3% TBSA, and mean length of hospital stay was 27.0 days. Approximately 26.3% were suspected of having an inhalation injury, and this was confirmed by either bronchoscopy or clinical course in 88.6% of this subgroup. Mortality in patients arriving intubated was 30.8%, and these were excluded from the rest of the analysis. In the surviving 879 intubated patients, reasons reported by PBCPs for intubation included "airway swelling" in 34.1%, "prophylaxis" in 27.9%, and "ventilation or oxygenation needs" in 13.2%. Of these patients, 16.3% arrived directly from the scene, with the remainder arriving from another hospital facility. Of all survivors who arrived intubated, 11.9% were extubated on the day of admission, 21.3% were extubated on the first postburn day (PBD), and 8.2% were extubated on the second PBD. No patients who were extubated on PBD1 or PBD2 had to be reintubated. A significant number of burn patients have their initial airway management by PBCPs. Of these, a significant number are extubated soon after arrival at the burn center without adverse sequelae. Rationale for their initial intubation varies, but education is warranted in the prehospital community to reduce unnecessary intubation of the burn patient.

Any thoughts or input?

How can we better educate our selves and fellow prehospital providers on this topic?

Research: Prehospital Thrombolysis

2010-08-09T13:00:00.000-04:00

Check this out...

Also a topic within The EKG Club

Emerg Med J. 2010 Aug 3. [Epub ahead of print]
Paramedic decision making: prehospital thrombolysis and beyond.
Smith AM, Hardy PJ, Sandler DA, Cooke J.

Abstract

Background Mortality from acute myocardial infarction is influenced by the speed at which reperfusion therapy is delivered. In the UK, prehospital thrombolysis (PHT), administered by paramedics, has been developed to improve call to needle (CTN) times. Recently, it has been shown in randomised trials that mortality can be further reduced by primary percutaneous coronary intervention (PPCI). This project was developed to assess current ST-elevation myocardial infarction practice in a district general hospital and to prepare paramedics for PPCI. Methods Data were collected prospectively over a 12-month period for all patients who received thrombolysis for a presumed myocardial infarct. The primary outcome measures for each case were who delivered the thrombolysis, either the paramedic crew or the hospital, and if the patient did not receive PHT the reason why not. Secondary outcome measures included the CTN time. Results 153 patients received thrombolysis over the time period (99 men, 54 women, mean age 66+/-15 years). Of this group, 55 patients received PHT (35.9%) with a median CTN time of 36 min (inter-quartile range (IQR) 30-42 min). The commonest reason for exclusion from receiving PHT was that the patient's history did not fit the eligibility criteria (25% of cases). Conclusions Paramedics are able to deliver PHT promptly and safely. With the focus now on PPCI, it is anticipated that not only will paramedics be able to select patients for delivery to a heart attack centre for PPCI, they will be selecting many more patients for this treatment than have up to now received PHT.

So, what do you think? Are you ready to start administering clot busters? Here is another abstract that concludes that the early identification of STEMI improves patient outcomes.

Am J Cardiol. 2009 Apr 1;103(7):907-12. Epub 2009 Feb 7.
Effect of prehospital triage on revascularization times, left ventricular function, and survival in patients with ST-elevation myocardial infarction.
Sivagangabalan G, Ong AT, Narayan A, Sadick N, Hansen PS, Nelson GC, Flynn M, Ross DL, Boyages SC, Kovoor P.

Abstract

Shorter reperfusion times lead to better outcomes in patients with ST-elevation myocardial infarction (STEMI). We assessed the efficacy of prehospital triage with bypass of community hospitals and early activation of the cardiac catheterization team on revascularization times, left ventricular (LV) ejection fraction, and survival. Patients with STEMI (624) were divided into 3 groups determined by site of triage: ambulance field triage (163), interventional center emergency department (202), and 3 community hospital emergency departments (259). Compared with community hospital and interventional center triages, ambulance field triage resulted in a significant median decrease in door-to-balloon times of 68 and 27 minutes, respectively (p <0.001). LV ejection fraction was highest in the field triage group (52 +/- 13%) compared with the interventional center (49 +/- 12%) and community hospital (48 +/- 12%, p = 0.017) groups. Thirty-day mortality was lowest in the ambulance field group (3%) compared with the interventional facility (11%) and community hospital (4%, p = 0.007) groups. There was a significant difference in long-term survival with up to 30-month follow-up among the 3 triage groups (p = 0.041). With time-dependent Cox regression modeling the difference in survival was significant only during the first week after STEMI (p = 0.020). Every extra minute of symptom onset to reperfusion time was associated with a relative risk of long-term mortality of 1.003 (95% confidence interval 1.000 to 1.006, p = 0.027). In conclusion, field triage of patient with STEMI decreased revascularization times, which preserved LV function, and improved early survival.

And another advocating statement from 2007:

J Emerg Med. 2008 May;34(4):405-16. Epub 2007 Dec 27.
The role of fibrinolytics in the prehospital treatment of ST-elevation myocardial infarction (STEMI).
Sayah AJ, Roe MT.

Abstract

The efficacy of fibrinolytics in the treatment of ST-elevation myocardial infarction is directly related to the time of administration, with the first 2 h after symptom onset seen as a critical period for greatest improvement in cardiovascular parameters and mortality. The American College of Cardiology/American Heart Association recommends a medical contact to treatment time of 30 min for fibrinolysis in patients with ST-elevation myocardial infarction. In selected patients, reperfusion goals may be expedited with prehospital administration of fibrinolytics. In clinical trials, prehospital fibrinolysis markedly reduced the time from symptom onset to treatment, allowed earlier ST-segment resolution, and reduced short- and long-term mortality compared with in-hospital treatment. Prehospital fibrinolysis has become more feasible with the introduction of prehospital 12-lead electrocardiography, improved skills of emergency medical services personnel, improved communication with the Emergency Department, and the advent of bolus fibrinolysis. Rapid and accurate administration of a fibrinolytic is vital for the success of prehospital fibrinolysis.

Okay, that one is a bit old. Lets open the discussion on this topic. Let me know what you think. Provide some better research, and I will tell you now... there is some out there. I'd also like to hear from anyone out there that has been a part of a thrombolysis trial.

Thanks for your participation,

Adam Thompson, EMT-P

Research: Pediatric Pain Management

2010-08-08T22:28:00.000-04:00

Check this out...

Am J Emerg Med. 2010 Aug 2. [Epub ahead of print]
Out-of-hospital emergency medicine in pediatric patients: prevalence and management of pain.
Galinski M, Picco N, Hennequin B, Raphael V, Ayachi A, Beruben A, Lapostolle F, Adnet F.

Abstract

INTRODUCTION: Much less is known about pain prevalence in pediatric patients in an out-of-hospital than emergency department setting. The purpose of this study was to determine pain prevalence in children in a prehospital emergency setting and to identify the factors associated with pain relief. MATERIALS AND METHODS: This prospective cohort study in consecutive patients 15 years or younger was conducted by 5 mobile intensive care units working 24/7 (January-December 2005). The presence of pain, its intensity, and alleviation by the administration of analgesics were recorded. RESULTS: A total of 258 of 433 pediatric patients were included, of whom 96 were suffering from acute pain (37%; 95% confidence interval [CI], 31-43) that was intense to severe in 67% of cases. Trauma was the only factor significantly associated with acute pain (odds ratio, 818; 95% CI, 153-4376). Overall, 92% of the children in pain received at least one analgesic drug; 41% received a combination of drugs. Opioid administration was significantly associated with intense to severe pain (odds ratio, 7; 95% CI, 2-25). On arrival at hospital, 67% of the children were still in pain; but 84% had experienced some pain relief regardless of their sex, age, or disorder. CONCLUSION: In a prehospital emergency setting, more than a third of children experience acute pain with a high prevalence of intense to severe pain. Scoring pain in children, and especially in the newborn, is beleaguered by a lack of suitable scales. Despite this, it was possible to treat 90% of children in pain and provide relief in 80% of cases.

If we could only get these numbers with our adult patients. I can't help but believe this is due to a couple main factors. 1. We inherently want to make kids feel better & 2. We are pretty sure that our pediatric patients aren't drug seekers.

Here is some advice, treat adult patience that have pain as if they were pediatric patients that have pain. Just make sure you adjust the dose proportionately. This is not an attempt to be cynical, yet just the opposite. I am attempting to remove all cynical notions preventing appropriate pain management.

Grand Rounds - 3

2010-08-07T10:51:00.000-04:00

The August edition of Grand Rounds is now up over at EMSResponder.com. Click here to check it out.

Peter Pronovost - The Science of Safety

2010-08-04T14:19:00.003-04:00

As some of you may know, Crew Resource Management is an area of interest for me.

While the following videos don't specifically mention Crew Resource Management, the techniques discussed are very much related to Crew Resource Management.

This is worth your time.

Advocating Airway Education

2010-07-29T19:13:00.005-04:00

In the popular and acclaimed JEMS article Experts Debate Paramedic Intubation, there were a few key points made that I would like to elaborate on, as well as provide some of my own insight from the research I have come across.

Key Point 1

Endotracheal Intubation has been best performed by those who maintain experience and those whom utilize Rapid Sequence Induction/Intubation.

Experience should be maintained in a number of manors:

Operating room rotations
Mannequin scenarios (without the dummy supine on a table)
Cadavers if possible

Rapid Sequence Induction is when one of many combinations of sedatives and paralytics are used to facilitate endotracheal intubation. This is a high risk procedure with many possible complications. It requires more education, and practice.

Dr. Bledsoe: Do you feel there’s a role for RSI in the prehospital setting? Dr. Wayne, I know your program has decades of success with RSI. What do you think?

Dr. Wayne: Although there are no nationally defined indications for the use of RSI in the field, we at Whatcom Medic One believe that RSI is indicated for any patient in whom there’s a need to control an “uncontrolled” airway. This may include depressed GCS score, excess secretions, hypoxia that may be correctable, ventilatory fatigue or central nervous system depression with or without secondary respiratory depression.

Dr. Tan: I believe there is, but it must be in the right context with requisite oversight and extraordinary training. I oversee more than 100 paramedics in my system, yet only 10 of them have RSI privileges. They’re required to obtain critical care certification, attend ongoing training sessions with me every 12 weeks, attend annual specialized training courses and undergo 100% audits of their critical care trips. It’s a strenuous and time-consuming process but one that can’t be overemphasized given the complexity and danger inherent to RSI. I certainly don’t believe RSI should be a “routine” part of any standing orders, as there is nothing routine about it.

Dr. Wang: I think RSI should be restricted to the aeromedical setting for use by critical care flight nurses and/or flight medics for the reasons I’ve previously detailed. I really challenge those medical directors who currently allow RSI and promote its use in other systems. Although I applaud their efforts and attention to quality improvement and training, they still equate successful intubation with a positive outcome. As Dr. Eckstein said, in the absence of prospective RCTs, we can’t assume that prehospital RSI has actually improved outcomes for our patients.

Dr. Eckstein: RSI is potentially useful where paramedics have exceptional skill, training and medical oversight. Unfortunately, this is a tiny fraction of EMS agencies. If we replaced the “I” (intubation) with “A” (airway—Combitube, King, etc.), this might relieve much of the angst over prehospital RSI.

Key Point 2

Airway Management ≠ Endotracheal Intubation (ETI)

What I mean by that, is that just because a patient's airway requires management, it does not mean that ETI is the only option.

Questions to ask:

Is there a risk for aspiration?
Is the patient ventilating on their own?
Is the patient oxygenating on their own?
Is the patient conscious?
How difficult will this ETI attempt be?
What is my backup plan?

Other options:

Bag-valve mask (possibly with an OPA/NPA)
Combi-tube
King LT/LTD
Laryngeal Mask Airway

Dr. Bledsoe: Are the alternative airway devices (e.g., King LT, etc.) good enough for prehospital airway management?

Mr. Gandy: Yes. The studies have shown that excellent ventilation can be achieved with these devices.

Key Point 3

The #1 way to confirm proper placement of the endotracheal tube in the field is end-tidal CO2 (ETCO2). If you have ETCO2 available in the field, use it.

ETCO2 measures the amount of CO2 that is being exhaled by the patient. This lets us know that the O2 we are putting into the body is being used and exchanged for the CO2 that comes out via pulmonary perfusion. This exchange occurs in the lungs, which just so happens to be the place that we are attempting to ventilate.

Key Point 4

Anticipate the difficult airway.

Mr. Gandy: The biggest problem is inadequate training and practice in airway evaluation, such as using the Malampatti or Cormack-Lehane criteria; using aids to intubation, such as bougies; the BURP maneuver; alternative laryngoscope techniques, such as the “skyhook” technique; and a good assortment of alternative airway devices, including either GlideScope or AirTraq. Ventilation should be emphasized over intubation, and extensive practice with BVM ventilation should be required.

Malampatti scoring is done by having the patient stick out their tongue. The difficulty of the proceeding ETI attempt can be gauged by the visibility of the oropharynx.

Don't aim for jewelry!

Cormack-Lehane Citeria is utilized with direct laryngoscopy. This is done by visualizing the vocal cords and making note of how much of the opening is visible:

Grade 1, visualization of the entire laryngeal aperture;
Grade 2, visualization of parts of the laryngeal aperture or the arytenoids;
Grade 3, visualization of only the epiglottis; and
Grade 4, visualization of only the soft palate.

Bougie - This is almost like a super long rigid stylet that is introduced through the vocal cords first. You then thread the ET tube over it.

BURP Maneuver - Backward, Upward, Rightward, Pressure of the larynx.

Don't worry if you don't understand the picture above. It is just a step by step of the BURP maneuver. Basically you place your fingers on the palpable cricoid ring of the patient. Push towards their posterior, and slightly towards their right. This should bring the trachea and it's structures to the best point of view during direct laryngoscopy.

"Skyhook" - I believe Gandy is referring to what my peers and I call the "fish hook" maneuver. This is reserved for the more hefty patients that may be hard to intubate.

This is a two person procedure. One person is dedicated to laryngocopy, and the other will direct person 1, visualize the vocal cords, and pass the ET tube.

Person 1 - With Laryngoscope and a Macintosh blade

- Straddle the supine patient
- Hook the blade into the mouth
- Pull back, keeping the blade off of the teeth
- Make adjustments based off person 2's direction

Person 2 - With appropriately sized ET Tube

- Position yourself at patient's head
- Direct person 2 until the vocal cords are visible
- Pass ET tube

I spoke about the Glidescope in my post Video Laryngocopy. Go check it out.

Key Point 5

It doesn't end after the intubation is accomplished.

Once you've got the tube, you should aim all of your efforts at keeping the tube and ventilating ACCURATELY. Using a mechanical ventilator after the ET tube is placed provides the ability to set an accurate rate and tidal volume. If one is not available, ETCO2, and O2 saturation should guide your ventilation rate and tidal volume.

Place a cervical collar on the patient to limit their movement.

Make note of the depth,

Monitor diligently.

It isn't the end of the world if you lose the tube. It may be the end of your career if you don't realize it.

Please see Post-Intubation Tracheal Stenosis for yet another consideration.

58 year old female CC: Chest pain - Conclusion

2010-07-29T10:31:00.002-04:00

Here's the conclusion to the 58 year old female with chest pain and left bundle branch block.

To refresh your memory here is the 12-lead ECG.

And for those of you who requested lead V4R.

This ECG meets all 3 of Sgarbossa's criteria to identify acute STEMI in the presence of left bundle branch block.

Keep in mind, it only has to meet one criterion in one lead!

(Please note: One criterion has been modified from its original form. Instead of discordant ST-elevation > 5 mm we are looking for discordant ST-elevation > 0.2 the depth of the S-wave. Credit to Dr. Smith of Dr. Smith's ECG Blog.)

Angiography revealed 100% occlusion of the LCX and 99% occlusion of the RCA.

Thanks to everyone who commented on the case!

See also:

AMI in the presence of LBBB - Sgarbossa's Criteria Part I

AMI in the presence of LBBB - Sgarbossa's Criteria Part II

Sgarbossa's criteria - new graphic

"New" LBBB - What's the big deal?

Discordant ST-Segment Elevation in LBBB or Paced Rhythm

58 year old female CC: Chest pain

2010-07-25T21:27:00.002-04:00

Here's another case study from an international reader who wishes to remain anonymous.

Presenting Complaint - Chest Pain

History of Present Complaint - 58 year old female, nil cardiac history, mild smoker, social drinker and overweight.

Complaining of acute central chest pain @ rest. Awoken by pain.

On Arrival - Sat upright on settee (Editor's note: One of you Brits will have to interpret that for me!)

On examination:

Alert, orientated and communicable (GCS 15)
Pale, cool dry skin.

Nil SOB, clear bi-lateral air entry - nil adventitious breath sounds
R/R 19, SpO2 99%

H/R 68 and irregular, BP 125/74

Temp 36.8
B.M 7.2 (Editor's note: B.M. is BGL measured in millimoles. 1 mmol/L of glucose is equivalent to 18 mg/dL. Hence, this patient's sugar is about 130).

C/O chest pain.

O - Acute. Awoken from sleep.
P - Nothing makes pain better. Not affected by breathing
Q - Non specific compressing type pain
R - Central chest pain radiating left arm
S - Pain score 6/10
T - 30 mins
I - No pain intervention sought.

Slight nausea, nil vomit

The cardiac monitor is attached.

A 12-lead ECG is captured.

Once again, I am impressed at the power of Web 2.0.!

Getting case studies like this from thousands of miles away is a real privilege and it makes me very happy to be able to share them with my colleagues from around the world!

This ECG meets all 3 of a certain criteria.

What criteria are we talking about and how would you treat this patient?

While you're at it, please CLICK HERE if you missed my previous post and cast your vote!

Chronicles of EMS - Here Are the Finalists! VOTE NOW!

2010-07-23T10:01:00.000-04:00

As you may have heard, the finalists are in for the Chronicles of EMS "Change the Name" competition! The field has now been narrowed from over 500 entries to just 5!

It just so happens that my girlfriend Kelly is one of the finalists.

Now, I don't want to influence your decision in any way....

So please CLICK HERE to cast your vote NOW!

Select one of the following:

Beyond the Lights and Sirens

Mobile Medicine

Frontline Medicine

Medicine in the Streets

Real Life, Real Emergencies

Again, just choose from your heart.

Don't be influenced by the fact that this could lead to a trip to Europe for yours truly! :)

See also:

Chronicles of EMS - "Change the Name" Competition!

Grand Rounds - 2

2010-07-17T11:25:00.000-04:00

In an effort to spread the knowledge of EMS blogs, I am authoring a monthly column on EMSresponder.com.

Check out Grand Rounds. The first one is more of an introduction to EMS blogs. Next month I will summarize the posts a bit more. If you are interested in me mentioning your blog, shoot me an email at paramedicine101@gmail.com.

Intubation Education

2010-07-10T16:33:00.008-04:00

In the article I was writing about^[1] (Experts Debate Paramedic Intubation) in my post Experts Debate Paramedic Intubation - JEMS.com, there is a bit of defense of the status quo in intubation and intubation training.

We get hung up on many of the same problems. We think that there is one right way to do things, rather than accept that we are adapting what we do to the different circumstances we are faced with.

We act as if the OR (Operating Room) is the only place that we can obtain good practice. There is no evidence to support this.

There is nothing to show that OR training is superior to morgue training and mannequin training, but we act as if the decreased availability of OR time is the only reason medics can't intubate competently.

We act as if the only problem with the way we are teaching paramedic school is that the students are not learning. As if this is not a reflection on the teaching.

Teaching means providing information to students in a way that helps the students to understand. If the students do not understand, the teacher did not teach.

Perhaps you do not believe that we do a poor job at intubation education.

Results

Nine hundred twenty-six patients had an attempted intubation. Methods of airway management were determined for 97.5% (825/846) of those transported to a hospital and 33.8% (27/80) of those who died in the field. For transported patients, 74.8% were successfully intubated, 20% had a failed intubation, 5.2% had a malpositioned tube on arrival to the ED, and 0.6% had another method of airway management used. Malpositioned tubes were significantly more common in pediatric patients (13.0%, compared with 4.0% for nonpediatric patients).

Conclusions

Overall intubation success was low, and consistent with previously published series. The frequency of malpositioned ETT was unacceptably high, and also consistent with prior studies. Our data support the need for ongoing monitoring of EMS providers' practices of endotracheal intubation.^[2]

Those numbers may be considered good in many areas - batting average, picking winning stocks, votes in an election. When it comes to airway management, we would be more appropriate if we described failure rates.

These failure rates are unacceptably high.

Overall intubation success was low, and consistent with previously published series.

In other words, the authors believe that this is the expected result of the way we train paramedics to intubate.

Can anyone show that this is not true?

The frequency of malpositioned ETT was unacceptably high, and also consistent with prior studies.

This is the expected result of the way we train paramedics to intubate.

Our data support the need for ongoing monitoring of EMS providers' practices of endotracheal intubation.

5.2% had a malpositioned tube on arrival to the ED.

5.2% Unrecognized Esophageal Intubations!

~~Ongoing monitoring~~ Watching is not enough.

We need to dramatically change the way we handle intubation education.

Footnotes:

^[1] Experts Debate Paramedic Intubation - Should paramedics continue to intubate?
JEMS.com
Bryan E. Bledsoe, DO, FACEP, FAAEM | Darren Braude, MD, MPH, FACEP, EMT-P | David K. Tan, MD, FAAEM, EMT-T | Henry Wang, MD, MS | Marc Eckstein, MD, MPH, FACEP | Marvin Wayne, MD, FACEP, FAAEM | William E. Gandy, D, LP, NREMT-P
Thursday, July 1, 2010
Article

^[2] A prospective multicenter evaluation of prehospital airway management performance in a large metropolitan region.
Denver Metro Airway Study Group.
Colwell CB, Cusick JM, Hawkes AP, Luyten DR, McVaney KE, Pineda GV, Riccio JC, Severyn FA, Vellman WP, Heller J, Ship J, Gunter J, Battan K, Kozlowski M, Kanowitz A.
Prehosp Emerg Care. 2009 Jul-Sep;13(3):304-10.
PMID: 19499465 [PubMed - in process]

.

Videos: Kill some time

2010-07-08T16:15:00.001-04:00

I'm going to be on vacation for a week, in Chicago. In the meantime, here are some videos to kill some time. I am not responsible for the content.

Treating Tachycardia

2010-07-05T20:15:00.004-04:00

Treating Tachycardia

By Adam Thompson, EMT-P

Tachycardia simply means a faster heart rate than normal. With the sinoatrial node, which is the heart's inborn pacemaker, the intrinsic rate is between 60 and 100 beats per minute. When the rate exceeds 100 beats per minute, tachycardia is present.

When treating tachycardia, it is important to first consider a compensatory cause. The body tends to use an increased heart rate as a frequent compensatory mechanism when it senses decreased perfusion. Two of the best dysrhythmics in the EMT and paramedic's tool box are OXYGEN and NORMAL SALINE. Both of these treatments should be attempted prior to using any other medication. It is not advantageous to eliminate a compensatory tachycardia in a patient who needs it to perfuse. Locating the cause of the decreased perfusion would be optimal.

Another thing to consider is the patient's hemodynamic stability. With organized tachycardic rhythms in unstable patients, synchronized cardioversion is indicated. There seems to be a fear amongst prehospital providers when it comes to shocking people. The paramedic seems to be much more comfortable giving anti-arhythmic/dysrhythmic medications than they do performing cardioversion. This is in-fact backwards thinking. Consider Kelly Grayson's outlook on dysrhythmic drugs--they are selective cardiotoxins. First off, they are not naturally found in the body. Second, they metabolize over time and the reaction can be unpredictable. Thirdly, they are used to counteract cellular depolarization. Do you know what happens in the absence of cellular depolarization in the myocardium? Asystole--not a common side effect, but it drives home the point doesn't it?. Other complications, like high-grade atrioventricular blocks, and long QT syndrome may also occur. Conversely, synchronized cardioversion doesn't have nearly as many unwanted effects. It works fast, and goes away. The medication you should be considering, is some sort of sedative or benzodiazapine prior to cardioversion.

Next, after determining the patient's hemodynamic stability, the width of the QRS should be considered. If the patient is stable, and they are in a sustained tachycardia, dysrhythmic medications can be considered. It is important to determine the width of the QRS, because medications like Cardizem (diltiazem), or Adenocard (adenosine) that may be administered to narrow complex rhythms, can effectively KILL people with wide QRS rhythms. Notice that there is not a 'ventricular tachycardia' algorithm? It states 'Wide QRS', and lists 'uncertain rhythm' below. This is an important concept. If it is wide, and you are uncertain of the origin, it is ventricular tachycardia until conclusively proven otherwise. Another reason that it is a WCT guideline and not a ventricular tachycardia guideline is because of conditions like WPW (wolff parkinson white syndrome). With WPW, a delta wave may be present causing widening of the QRS complex. This is important because adenosine, and Cardizem should not be administered to patients with WPW. There is controversy regarding whether Amiodarone is safe with WPW, but as of now the American Heart Association considers it a safe option.

A wide QRS complex is considered greater than 120 ms or 0.12 seconds or 3 small boxes.

Points to remember:

O2 & fluids for compensatory tachycardia
Synchronized cardioversion is the SAFER option
If QRS is wide treat as V-tach

Note: Torsades de Pointes should not be treated with Amiodarone. This can cause lengthening of the QT interval, and subsequently a worse arrhythmia.

Brugada Criteria. This should only be used to confirm ventricular origin. Not to rule it out.

View more documents from Adam Thompson.

Videos: Acute Coronary Syndrome

2010-07-04T20:08:00.003-04:00

Some stuff for you visual learners, enjoy.

This one ends abruptly, but makes a point that I like to stress, DIAPHORESIS is BAD!

Sorry for this one, but I thought it was funny

In the following video, the presenter has used some of Tom B's teaching aids to teach Sgarbossa's criteria. I pronounce it with the 'S' by the way.

Also check these out - video , & video

Drug Profile: Ketamine

2010-07-04T12:44:00.007-04:00

Ketamine

By Adam Thompson, EMT-P

Since my beginning in the world of prehospital medicine, which wasn't too long ago, I have heard more and more about a particular drug. I have attended critical care and emergency medicine conferences and the same has been true. Ketamine seems to have become a favorite amongst many physicians. I have never administered the drug myself, but it has made its way into some prehospital standing orders, and with reason.

Ketamine Hydrochloride

Non-barbiturate anesthetic

Mechanism of action:

Creates a state of dissociation from reality.
Catecholamines (epinephrine & norepinephrine) are released.
Spinal reflexes are reduced.

Indications:

Indicated for anesthesia when cardiovascular depression must be avoided.
A commonly used induction agent to facilitate endotracheal intubation.

Contraindications:

Hypersensitivity to Ketamine
Increased intracranial pressure
Hypertension
Aneurysm
Thyrotoxicosis (hyperthyroid)
Congestive heart failure
Angina
Psychotic disorders
Pregnancy

So there are a lot of contraindications that happen to be conditions that we see commonly. But think about what they are, and what the side effects are of the other drugs that we administer for similar indications. Almost every other medication decreases blood pressure. Ketamine actually increases it, so it has its place.

Side Effects:

Hallucinations
Vivid dreams
Hypertension
Increased cardiac output
Tachycardia
Paradoxical direct myocardial depression
Increased ICP
Tonic-clonic movements

Overdose:

With high doses or rapid administration, respiratory depression may occur.

Dosage:

Oral: Pediatric 6 - 10 mg/kg
Intramuscular: 3 - 8 mg/kg
Intravenous: Pediatric 0.5 - 2 mg/kg, Adult 1 - 4.5 mg/kg

Onset is about 1-2 minutes if given I.V., and 3-8 minutes if given I.M.

Some research:

The effect of combined treatment with morphine sulphate and low-dose ketamine in a prehospital setting [1]

Conclusion

We conclude that morphine sulphate with addition of small doses of ketamine provide adequate pain relief in patients with bone fractures, with an increase in systolic blood pressure, but without significant side effects.

Anesthesia in prehospital emergencies and in the emergency department. [2]

Abstract

PURPOSE OF REVIEW: Recently, notable progress has been made in the field of anesthesia drugs and airway management. RECENT FINDINGS: Anesthesia in prehospital emergencies and in the emergency department is reviewed and guidelines are discussed. SUMMARY: Preoxygenation should be performed with high-flow oxygen delivered through a tight-fitting face mask with a reservoir. Ketamine may be the induction agent of choice in hemodynamically unstable patients. The rocuronium antagonist sugammadex may have the potential to make rocuronium a first-line neuromuscular blocking agent in emergency induction. Experienced healthcare providers may consider prehospital anesthesia induction. Moderately experienced healthcare providers should optimize oxygenation, hasten hospital transfer and only try to intubate a patient whose life is threatened. When intubation fails twice, ventilation should be performed with an alternative supraglottic airway or a bag-valve-mask device. Lesser experienced healthcare providers should completely refrain from intubation, optimize oxygenation, hasten hospital transfer and ventilate patients only in life-threatening circumstances with a supraglottic airway or a bag-valve-mask device. Senior help should be sought early. In a 'cannot ventilate-cannot intubate' situation, a supraglottic airway should be employed and, if ventilation is still unsuccessful, a surgical airway should be performed. Capnography should be used in every ventilated patient. Clinical practice is essential to retain anesthesia and airway management skills.

Pre-hospital use of ketamine for analgesia and procedural sedation [3]

Abstract

The safe delivery of adequate analgesia and appropriate sedation is a priority in prehospital care. The use of ketamine is described for analgesia and sedation in 1030 trauma patients in a physician-led prehospital trauma service. Ketamine was mainly used in awake non-trapped patients with blunt trauma for procedural sedation and analgesia. Detailed database searches did not demonstrate loss of airway, oxygen desaturation or clinically significant emergence reactions after ketamine administration. Ketamine is relatively safe when used by physicians in prehospital trauma care.

Ketamine for prehospital use: new look at an old drug. [4]

Abstract

INTRODUCTION: Ketamine has been used extensively for analgesia and anesthesia in many situations, including disaster surgery where extra personnel and advanced monitoring are not available. There are many features of ketamine that seem to make it an ideal drug for prehospital use. The reported use of ketamine in the prehospital environment is limited, however. The purpose of this study is to review the experience in the use of ketamine in a regional air ambulance service and suggest indications for its use in the prehospital setting. METHODS: This was a retrospective study of all patients transported by a regional aeromedical program. Patients were included in this study if the crew had used ketamine at any time during the flight. Data regarding the transport collected included patient age, type of transport, indications for ketamine use, and adverse reactions. RESULTS: During the period studied, ketamine was used in 40 patients. The age range was 2 months to 75 years. The indications and situations requiring use were varied and included both trauma and medical patients. Hypotension with need for analgesia, agitation or combativeness and intact airway, or pain unresponsive to narcotic medications were the most common indications for use. Ketamine was used both intravenous and intramuscular, even without intravenous access. There were no adverse reactions. CONCLUSIONS: Ketamine is an ideal drug for use in many prehospital situations. Our experience suggests that it is safe, effective, and may be more appropriate than drugs currently used by prehospital providers.

ClinCon 2010

2010-07-02T11:55:00.001-04:00

Hello to all of our loyal readers. It's Adam here and I am sorry for the long periods of nothing to read. It was that time of year again, and I was preparing for the ClinCon conference. If you are unfamiliar with it, head over to their WEBSITE.

The reason this takes up so much of my time is because I am part of my agency's ALS competition team. We compete in these scenario-based competitions. It's somewhat of a game. Imagine the worst possible call you could ever run, and multiply that by five. That tends to be the types of scenarios the sadist that come up with the challenges think up.

This was my fourth year competing at ClinCon and my team had remained winless. There are two days of competitions with some of the best teams in the country competing. On the first day is the preliminary round, which every team competes in. A team is made of three crew members, and one alternate whom usually holds the video camera.

Preliminary scenario

Bus crash:

The first five minutes was a START Triage scenario which required each team to go through a number of cards that included patient type and vital signs. Each card had a number and you had to assign a color (red, yellow, green, or black) to the corresponding numbers.
We are then rushed in, to what is deemed the yellow treatment area. Within this area was a mother holding a baby, and a patient complaining of burning eyes.
A good sample history and assessment uncovers the cause of the burning eyes which is chlorine. The patient also presented with wheezing.
The baby was who was actually a green, was not suppose to be re-triaged, but kept with mom instead.
The mother ends up having hypertension, and then postpartum eclampsia. Her seizures would persist until Magnesium was administered.
At about the ten minute mark, another patient presents. He is nearly unresponsive, and shows signs of a cardiac contusion and cardiac tamponade.

Treatments they were looking for:

Rapid full-body assessments on every patient.
Re-triage all patients red.
Flush eyes of chlorine exposed patient
Treat wheezing with bronchodilator
Once wheezing subsides rales present - treat with Lasix or CPAP
Treat Eclampsia with Magnesium Sulfate
Recognize pericardial tamponade

Treatments we did:

Got 100% of the assessments
Flushed eyes of chlorine exposure
Provided high-flow O2, then albuterol, the nebulized Sodium Bicarbonate.
Recognized the low acuity of the baby and kept it with mom
Treated mom with benzodiazepines then Mag.
Recognized Beck's triad & electrical alternans (cardiac tamponade) and performed a pericardiocentesis.

So we didn't do exactly everything that they were looking for. Even though we completely resolved the tamponade, there were no points for the percardiocentesis because they said "no one does that". Um, we do. In fact, all arrest thought to be due to blunt force thoracic trauma receives three needles in their chest. One of them in the heart.

We were concerned that the other 40 teams would have done better and we wouldn't make it into the top five this year. This concern subsided once we saw the results. We got second over all and made it into the finals once again. Even though, this is just a scenario-based competition and not a real sport, there is a lot of pride. These teams that compete in these challenges take it very seriously and are impressively good. We were thrilled to have done so well.

The Finals

Political rally:

The bus that crashed in the preliminaries was to be headed to a political rally that set the scene for the finals. The finals are performed in front of a live audience at the venue. Prior to entering the scenario, each team was shown a video. It is of the political rally, and portrayed a possible explosion.

Three initial patients.
A room filled with picket signs and full bottles labeled dihydrogen monoxide
A single black box about the size of a shoe box was present in the middle of the room.
First patient was in V-fib arrest, and had a dialysis shunt. CPR was being poorly performed by a distractor.

A distractor is any actor in the scenario that is not a patient. Dihydrogen monoxide = water.

Second is a patient with an avulsed eye from a possible explosion.
Third patient presented with an open mandibular fracture and signs of traumatic asphyxia.
At about 4 minutes, a fourth patient presented. He was yelling and deaf. He had signs of bilateral perforated tympanic membranes, or eardrums. He was yelling that his neck hurt.
At about five minutes three more patients walked in with burning eyes from being maced.

Sounds easy right? Well in twelve minutes it is a very stressful and high paced incident.

Treatments they were looking for:

Scene control
Assessments for every patient
V-fib arrest patient is to be defibrillated into a PEA
After PEA is present they expected you to determine hyperkalemic cause and administer sodium bicarbonate and/pr calcium chloride.
The eye avulsion only required BLS care
The traumatic asphyxia required a cricothyrotomy within five minutes.
Obtain SAMPLE history from deaf guy by writing it down
Flush the eyes of the maced individuals
DON'T OPEN THE BLACK BOX

If you opened the box, you became exposed to chlorine gas and had to flush your eyes before you could do anymore treatments. I am not going to go into the details of how every team performed or what exactly we did. All I am going to say is WE WON.

That's right, Lee County EMS, my team, got first place this year. So bragging rights are ours for the year, and then we will return for the competition once again. There are many other similar competitions to this throughout the country and I will be on EMS Educast this month to talk about them a little more.

So I am back and will be getting back to posting more often. You may have noticed the new look of the site. Tell me what you think. I am hoping to make the move soon to FIRE-EMS Blogs.

When All You Have is a Hammer, Every Problem Looks Like... Lasix?

2010-06-21T20:38:00.002-04:00

I posted this article over at http://www.lifeunderthelights.com/ a few days ago and I thought it would good for here as well. I'm sorry that I've only rarely posted here, but I read this blog quite often and recommend it to all of my peers. Enjoy

-----------------------------------------------

A few years ago I responded to a structure fire on the main engine out of my station. The fire was at a house that had been converted to a dog kennel and grooming shop just a few blocks away from the firehouse and was a short response time. It was a light-staffing day and we responded as a three person engine company. As the senior firefighter I was the acting company officer and my new girlfriend at the time, who just happens to be my wife now, was the backseat firefighter. Get ready for the “Awwww” moment… it was our first fire “as a couple”. There was a number of cool things that came out of the fire, but one of them was the fact that Gina grabbed *my* maul.

On our main engine, there’s an 8-pound maul (big hammer) that I grab as my tool of choice every time I jump off the truck for a fire. It just tucks so neatly in my SCBA’s belt and is so compact yet handy that I make a beeline for it every time. This time, Gina had taken it, so I grabbed a pick-head axe.

It’s amazing when I have my maul how every access problem looks like something that I can solve by whacking it with a hammer of some sort. On this fire, I learned that when one has an axe, every problem looks like it can be solved by some sort of chopping.

Moral of the story, Gina and I entered the structure, saved the pooches, and stopped the fire in its trucks with minimal damage. There’s actually a hilarious video that I believe is still on our department’s web site that I’d let you see if I didn’t hide the name of the department(s) I work for due to reasons of wanting to remain employed.

And, like a lot of posts I write, I told you that so I could tell you this about an EMS call I responded to an indeterminate amount of time ago. I have the honor and privilege to be the senior medic on most shifts I work and I precept a lot of students on the ambulance. This shift was no different and this 0-dark-30 call illustrates a point that I’d like to explain to you.

For this call, the primary ambulance out of our station responded because they were on the way back from another call and my partner and I responded in our ambulance because we were up on the alternating call rotation. They arrived at the poorly-accessible apartment complex a few minutes before we did and made first patient contact. As it turns out, the middle age patient had ran out of his/her prescription Lasix (a potent diuretic, or water pill) a week or so prior to the call and had been retaining a great deal of excess bodily fluid. The patient’s legs were markedly and grossly swollen and weeping fluid out of fluid filled blisters. The Patient called us because he/she could no longer stand the pain of the cellulitis (infection) that had developed. The patient had no respiratory compromise, his/her lungs were clear, and he/she really had no other complaints. The patient had an extensive medical history of organ failure and disease. He/she was fully alert and oriented, and was able to assist us as we simply picked him/her up and carried him/her to the cot.

As we were loading the patient up in the ambulance and I was about to get into the back to continue my assessment and treatment of the patient, the EMT from the other ambulance who happens to be an almost-done Paramedic student told me, “So those legs are the worst I’ve ever seen fluid wise, you’re going to push some lasix on this one”. I mumbled something and got into the truck. I was tired and wasn’t really able to form complete sentences at the time due to sleep deprivation. I continued my assessment where I found that the frail patient had a blood pressure in the 70 systolic range (Low!) and that in addition to retaining fluid in his/her legs, he/she was also retaining fluid in his/her abdomen and was probably in need of a paracentesis. I managed the patient with a (beautifully executed, I must say) IV stick into an impossibly small and crooked vein, and gave just enough fluid to bring his/her BP up a bit without adding to his/her fluid overload all that much. I put the Pt on oxygen and a cardiac monitor, which revealed a normal sinus rhythm without ectopy and obtained a 12-lead EKG as well, which was not indicative of any acute problems. The patient stated that his/her pain was managed by padding and positioning of his/her swollen legs and even though he/she complained of no breathing problems, I put him/her on a bit of oxygen via nasal cannula.

The transport was uneventful, although his/her blood pressure never did come up. The ER later diagnosed the Pt with complete liver failure and toxicity.

But the interesting part of the story is this, when I got back the medic student asked me about giving IV lasix to the patient, as we carry that in our medication stock and have it available as an emergency diuretic for patients in congestive heart failure and/or fluid overload with pulmonary edema and respiratory compromise. He was almost taken aback when I said that I didn’t give any.

I asked him if he did a full assessment. He said that he had tried… but that he didn’t have enough time before I arrived and we took the patient out to the ambulance. I gave him my assessment findings and the news of the very low blood pressure. He said that he agreed with me on not giving the lasix with the markedly low blood pressure but was curious when I explained that it wasn’t the reason I didn’t give the medication.

We in EMS, and especially new providers carry our own hammers… our treatments and medications that we’re able to give in the field. Medics that use these treatments more often are called “aggressive” and it is a badge of honor. In fact, in some cases, aggressive field treatment is indeed warranted and improves patient outcomes. However, in a lot of cases it is not indicated and patients benefit from what we don’t do more so than from what we could have done.

This patient didn’t have any respiratory compromise and while he/she obviously could have benefited from the dieresis or removal of the excess fluid, she didn’t meet the criteria for emergent field administration of lasix, which is respiratory compromise from pulmonary edema. I made the decision to let the physician evaluate the patient and determine the best treatment path that would fit in with the patient’s ultimate plan of care. I didn’t believe that the patient would ultimately benefit from my administration of lasix twenty minutes earlier than the ER could have done it if the physician so chose.

Every treatment we administer must be given with a full assessment of the risks and benefits to the patient for doing so. Every EMS person should familiarize themselves with the long-term care paths of the conditions we treat and try to maximize the long-term benefit to the patient with the acute and short-term care we give. Not every problem is “a nail” and sometimes the hammers we carry aren’t the best ultimate solution for excellent patient care. Remembering how we as EMS people fit into the grand scheme of the overall healthcare system and in the ultimate care paths of our patients will help us all to do what we’re supposed to do, which is to provide excellent and appropriate patient care.

It is also of note, I guess, that Gina rarely steals my maul anymore. Now that we’re married… I “give it freely” to her.. What’s mine is her’s, as they say.

--------------------------------------------

The original post has some pictures of the fire and of the doggies that my wife and I saved on our first "Fire Date" - It can be seen HERE

2010 AHA Updates

2010-06-14T00:30:00.005-04:00

It's that time again. As most of us Americans in the wide world of emergency medicine know, every five years the American Heart Association updates their recommendations. Those recommendations happen to be the standard for most prehospital agencies, and hospital systems. They say and we do. So what are we going to be doing now?

This year should not be bringing about any mega changes. The direction has stayed the same for the most part.

Where do the updates come from?

ILCOR - The International Liaison Committee on Resuscitation

Process for Evidence Evaluation

The publication of the 2010 International Consensus on Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) Science with Treatment Recommendations (CoSTR) will represent the scientific consensus of experts from a variety of countries, cultures and disciplines. Internationally recognized experts were brought together by the International Liaison Committee on Resuscitation (ILCOR) to evaluate and form an expert consensus on all peer reviewed scientific studies related to CPR.

To achieve this goals, ILCOR is conducting systematic reviews and updates of scientific evidence supporting resuscitation treatment recommendations. More than 500 resuscitation scientific topics will undergo evidence-based review. This process represents the most comprehensive, systematic review of the resuscitation literature to date.

The worksheets posted at this site represent the first step of an international consensus evidence evaluation process that will culminate in the publication of the 2010 International Consensus on CPR and ECC Science with Treatment Recommendations. In addition, resuscitation council-specific guidelines will also be published based on this international science consensus. Worksheet authors and expert reviewers worked very hard to present the information objectively.

The information contained in these worksheets will be presented and discussed between now and early 2010. In early 2010, the International CPR Consensus Conference will convene to allow final presentation and discussion of these worksheets, leading to evaluation and consensus by respective ILCOR Task Forces.
Readers are cautioned that these worksheets are a preliminary review and do not represent any ILCOR Task Force or Resuscitation Council recommendations.

ILCOR recognizes that the integrity of the evidence evaluation process depends on successfully managing real and perceived conflict of interest. ILCOR has policies in place to manage conflict of interest.
The 2010 evidence evaluation and science review process will culminate with the International CoSTR Conference in early 2010, in Dallas, Texas.

A separate publication covering guideline recommendations will be published by each resuscitation council.

So what does this all mean?

The AHA is part of an international committee that uses a systematic review system to scan through all the most valuable research available. The research is graded by how useful an unbiased it is, and then recommendations are made based upon a compilation of the results. The package all of this up in a nice-looking book, packed with a bunch of fancy flow charts, tables, and algorithms, and we buy it.

Link to the questions asked for 2010

Time of old

Amiodarone - Back in 2000 Amiodarone was given a class IIb recommendation from AHA. This was a push from, who else, the manufacturers of Amio. This happened synchronously with the changing of Lidocaine from a class IIb to an indeterminate rating. This occurred after a study showed that Amiodarone improved the number of cardiac arrest that regained pulses. This was accepted by many, and all the better, Amio works in atrial and ventricular arrhythmias--yippee.

The facts:

Amiodarone improved the amount of people that regained pulses, but not the amount of cardiac arrests that survived to discharge. No more people are surviving on Amio compared to Lidocaine. AHA knows this now, and has known this for a while.

AHA says that an "indeterminate" rating is no different from class IIb. So why the change? Because class IIb sounds a whole lot better when your selling a new drug.

So does this mean we are going back to lidocaine? Not sure, because there isn't any evidence that lidocaine is any better either--should we confuse everyone more? In fact, there is no evidence that any dysrhythmic does anything beneficial in cardiac arrest. That's right, no quality evidence supporting beneficial effects of dysrhythmics. Want some more? NO DRUGS administered in cardiac arrest have any supporting evidence!

Olasveengen TM, Sunde K, Brunborg C, et al. Intravenous drug administration
during out-of-hospital cardiac arrest. JAMA 2009;302:2222-2229.

Despite the traditional use of intravenous medications such as vasopressors and antiarrhythmics for victims of cardiac arrest, there is actually very little evidence to support these therapies. On the contrary, a recent multicenter center study demonstrated that the use of intravenous medications that are advocated in standard advanced cardiac life support (ACLS) guidelines was ineffective at improving survival of patients with out- of-hospital cardiac arrest (1). Olasveengen and colleagues now add further support to the contention that the use of intravenous medications in victims of non-traumatic cardiac arrest is not associated with improvements in meaningful outcomes. The authors performed a prospective randomized trial of consecutive adults with non-traumatic cardiac arrest that were treated within their emergency medical services (EMS) system in Oslo between 2003 2008. Patients were randomized to either receive standard ACLS therapies with intravenous drug administration (IV group) or ACLS therapies without any intravenous drugs (no IV group). A total of 851 patients were included in the study, 418 patients in the IV group and 433 in the no IV group. The researchers found there was an increase in survival to hospital admission with return of spontaneous circulation in the IV group vs. the no IV group (32% vs. 21%, P < 0.001). However, there was no difference between the IV group vs. the no IV group in terms of survival to hospital discharge (10.5% vs. 9.2%, P = 0.61), survival with favorable neurological outcome (9.8% vs. 8.1%, P = 0.45), or survival at 1 year (10% vs. 8%, P = 0.53). The results demonstrate that with the use of IV ACLS medications, patients simply die in the hospital rather than in the ED. Practically speaking, this amounts to increased intensive care unit bed utilization, hospital resource utilization, and expenses; but without any increase in meaningful survival. In this era of ED and hospital overcrowding and the increasing demand for cost-effectiveness in medical therapies, Stiell’s and Olasveengen’s studies should force us to consider that the use of IV medications for patients in cardiac arrest should be the exception rather than the rule…or guideline.

1. Stiell IG, Wells GA, Field B, et al. Ontario Prehospital Advanced Life Support Study Group. Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med 2004;351:647-656.

Back to Amiodarone 2010:

CONSENSUS ON SCIENCE:
Evidence from 1 RCT demonstrates the benefit of amiodarone over placebo for shock refractory or recurrent VT/VF for the endpoint of survival to hospital admission, but not to survival to hospital discharge. Retrospective trials show that lidocaine may be more beneficial than placebo, but selection bias mars these trials. In trials that directly compare amiodarone to lidocaine, patients administered amiodarone generally do better in short term results (ie survival to hospital admission), but no trial has shown an improvement in overall survival (Dorian P 2002 p884, Somberg J 2002 p853).

These trials were performed before the benefits of hypothermia was known, thus they did not incorporate this now proven therapy which improves survival after ROSC. Whether survival to hospital discharge and neurologic survival could be improved with amiodarone and subsequent hypothermia is not known. If that is the case then a stronger argument for amiodarone could be made; if that is not the case then an argument could be made to not give an AAD at all.

CPR Before Defibrillation

It was taught, back in 2005 by AHA, that we need to prime the pump. It was theorized that performing early defibrillation has no benefit because the heart was not being adequately perfused. This lead to a 2 minutes of CPR prior to shocking in an unwitnessed arrest rule. This is what we, who are AHA compliant, are doing.

CONSENSUS ON SCIENCE:
Two randomized controlled trials (LOE I) (Baker 2008 p424; Jacobs 2005 p39) demonstrated no improvement in ROSC or survival to hospital discharge in patients suffering out-of-hospital VF or pulseless VT who received CPR by EMS personnel for a period of 1.5 to 3 minutes before defibrillation, regardless of EMS response interval being greater or less than 5 minutes. One case series study (LOE IV) (Campbell 2007 p229) also failed to demonstrate improvements in ROSC or survival to hospital discharge with bystander versus no bystander CPR before defibrillation.
One randomized controlled trial (LOE I) (Wik 2003 p1389) and clinical trial (LOE III) (Cobb 1999 p1182) identified overall similar findings however improvements in ROSC, survival to hospital discharge and neurological outcome were observed in patients where the EMS response interval was greater than 4 to 5 minutes.

Evidence from one LOE 1 study (Wik 2003, 1389), one LOE 3 study (Cobb 1999, 1182) and five LOE 5 studies (Berg 2004, 1352; Kolarova 2003, 2022; Menegazzi 1993, 235; Menegazzi 2004, 926; Niemann 1992, 281) support the strategy to delay defibrillation to give BLS first for 1,5 to 8 minutes, in particular when the delay to ambulance arrival exceeds 5 minutes and no BLS is given before ambulance arrival. Evidence from two LOE 1 studies (Baker 2008, 424; Jacobs 2005, 39), one LOE 3 study (Campbell 2007, 229) and nine LOE 5 studies (Berg 2004, 1352; Yakaitis 1980, 157; Menegazzi 2003, 261; Menegazzi 2000, 31; Seaberg 2001, 301; Kolarova 2003, 2022; Niemann 2000, 543; Menegazzi 1993, 235; Rittenberger 2008, 155) do not support this strategy and are neutral. One LOE 5 study (Indik 2009, 179) gave direct evidence for the opposite strategy

Level of evidence - all that LOE stuff you see above is a reference to the grade the mentioned study received by the reviewer.

LOE 1
Randomised Controlled Trials:
These studies prospectively collect data, and randomly allocate the patients to intervention or control groups.

LOE 2
Studies using concurrent controls without true randomisation:
These studies can be:
· experimental - having patients that are allocated to intervention or control groups concurrently, but in a non-random fashion (including pseudo-randomisation: eg. alternate days, day of week etc), or
· observational – including cohort and case control studies
A meta-analysis of these types of studies is also allocated a LOE = 2.

LOE 3
Studies using retrospective controls:
These studies use control patients that have been selected from a previous period in time to the intervention group.

LOE 4
Case series: A single group of people exposed to the intervention (factor under study), but without a control group.

LOE 5
As with other categories of Levels of Evidence, we have used LOE 5 to refer to studies that are not directly related to the specific patient/population. These could be different patients/population, or animal models, and could include high quality studies (including RCTs).

So according to the evidence, we may need more evidence. However, there isn't much support to the current guidelines. Once again, do we change this back and confuse more people when we are uncertain if outcomes will improve?

Cardiocerberal Resuscitation or Cardiopulmonary Resuscitation?

Should EMS be doing chest compression only CPR? This is a good question when considering primary cardiac arrest. We know that primary respiratory arrest should involve aggressive airway management.

CONSENSUS ON SCIENCE
Six fair to good LOE 5 animal studies (Berg 1993, 1907; Berg 1997, 1635; Berg 2001, 2464; Ewy 2007, 2525; Kern 1998, 179; Kern 2002, 645) have shown comparable or better outcomes with continuous chest compression CPR as compared with interrupted compressions for ventilation in nonasphyxial cardiac arrest and in concept support such a change in resuscitation strategy. However animal models do not necessarily mimic the anatomical or arrest features of humans, and for these reasons arguably may be less applicable to human resuscitation. Clinical evidence from three retrospective cohort LOE 3 studies in adults suffering from cardiac arrest (Bobrow 2007, 1158; Kellum 2006, 335; Kellum 2008, 244) showed that provision of chest compressions in the absence of rescue breathing by trained professional (EMS) providers led to an improvement in survival to hospital discharge compared to provision of chest compressions with rescue breathing. However, these studies had methodological shortcomings that limit the ability to determine whether the improvements in survival were attributable to the provision of chest compression-only CPR in the absence of rescue breathing, including the lack of randomization, the implementation of other resuscitation protocol changes that may have affected outcomes, or simply a stronger clinical emphasis on the provision of good CPR. The remainder of clinical studies addressing this issue evaluated the outcome from continuous chest compression versus interposed ventilation CPR by untrained laypersons (bystander CPR),and did not directly address provision of care by trained professionals.

So there are studies out there, just maybe not enough--once again. There is also research on different compression:ventilation ratios showing promising data. Guess we will find out what really happens in October.

More of the same

There is a lot more evidence out there advocating chest compressions. No pulse checks, just compressions. More and more compressions. Push hard and push fast. Good chest compressions. Are you getting all of this?

Therapeutic hypothermia is gaining more popularity. The evidence is outstanding.

CONSENSUS ON SCIENCE:

Who to cool?
Evidence from one good randomized trial (LOE 1) (HACA, 2002, 549) and a pseudo-randomised trial (LOE 2) (Bernard, 2002,557) demonstrate improvement in neurological outcome after discharge from hospital in patients who had an out-of-hospital VF cardiac arrest, who were still comatose, and who were cooled within minutes to hours after return of spontaneous circulation to 32-34ºC for 12-24 hours. Two studies with historical control groups (LOE 3) showed improvement in neurological outcome after therapeutic hypothermia for comatose survivors of VF cardiac arrest (Belliard, 2007, 252; Castrejon, 2009, 733) One small (n = 30) randomized trial (LOE 1) showed reduced plasma lactate values and oxygen extraction ratios in a group (n =16) of comatose survivors after cardiac arrest with asystole or PEA who were cooled with a cooling cap (Hachimi-Idrissi, 2001, 275). Six studies with historical control groups (LOE 3) showed benefit after therapeutic hypothermia in comatose survivors of OHCA after all rhythm arrests (Bernard, 2007, 146; Oddo, 2006, 1865; Busch, 2006, 1277; Sunde, 2007, 29; Storm, 2008, R78; Don, 2009 3062). One studies with historical controls showed better neurological outcome after VF cardiac arrest but no difference after cardiac arrest from other rhythms (Bro-Jeppesen, 2009, 171). Two non-randomised studies with concurrent controls (Arrich, 2007, 1041; Holzer, 2006, 1792) indicate possible benefit of hypothermia following cardiac arrest from other initial rhythms in- and outof-hospital.

How to cool?
Nine case series (LOE 4) indicate that cooling can be initiated safely with intravenous ice-cold fluids (30 ml/kg of saline 0.9% or Ringer’s lactate) (Kliegel, 2005, 347; Kliegel 2007, 56; Bernard, 2003, 9; Virkkunen, 2004, 299; Kim, 2005, 715 ; Jacobshagen, 2009; Kilgannon, 2008; Spiel, 2009; Larsson, 2010;). Two randomised controlled trials (Kim, 2007, 3064; Kamarainen, 2009, 900), one study with concurrent controls (LOE 2: Hammer, 2009, 570) and three cases series (LOE 3) (Kamarainen,2008, 360;Kamarainen, 2008, 205) indicate that cooling with IV cold saline can be initiated in the pre-hospital phase.

More For Post-Arrest

There is evidence that patients who are resuscitated from primary cardiac arrest should be immediately cathed.

The significance of this new literature cannot be overstated. If further studies confirm these findings, it would strongly argue for enormous changes in prehospital systems of care to recommend that all survivors of primary cardiac arrest should be immediately transported to hospitals that have the capability of performing urgent PCI in conjunction with therapeutic hypothermia. Based on the current literature, it certainly seems advisable that emergency health care practitioners that care for resuscitated victims of primary cardiac arrest should engage in conversations with cardiology consultants and urge them to take an aggressive approach to PCI in these patients.

What does this mean for us? Post-arrest 12-lead ECGs for now. In the future, this may mean that we bypass non-PCI facilities with our post-arrest patients. If you think this will last long, you are wrong. Post-arrest patients are high dollar patients. Just think about all of the work-ups done on these patients. Don't think that the non-PCI hospitals won't be rushing to find a way around this. Will this mean more PCI centers? Probably not, because all of the other cardio-intervention seeking patients end up with big medical bills too--but who knows.

Shocking Stuff

So even though AHA came out and said that their initial recommendation for biphasic defibrillators is not backed by any evidence, there may be an actual benefit to having them. There is evidence supporting what I am about to tell you, but it may not make it into the 2010 update. I think it will though. It goes against what we have all learned. Remember "I'm clear, you're clear, we're all clear!"

There is no harm to a rescuer performing chest compressions, when defibrillation is performed using a biphasic monitor.

That's right. It has been said that more electricity passes through your body on one of those scales that checks your BMI than touching a patient when they are getting shocked. It has to be a biphasic defibrillator though.

So that's all so far. Go scan through the worksheets if you'd like. There is a ton of good research available. We can only assume, as of yet, what the final recommendations will be.

At the Florida Emergency Physicians' second annual symposium on critical care in the emergency department, Dr. Amal Mattu (yes, I am mentioning him once again) presented most of these updates. This motivated me to research and share them with you.

12-Lead Differential Diagnosis: Syncope

2010-06-10T14:51:00.004-04:00

12-Lead Differential Diagnosis: Syncope

By Adam Thompson, EMT-P

There are many causes of syncope. Syncope is the medical term for fainting. Most of us are pretty familiar with the common vasovagal cause. Fortunately syncope is often self-correcting; the patient hypo-perfuses, they blackout and fall, their body perfuses better, they wake up. This post will be dedicated to 12-lead presentations that may indicate causes of syncope.

I have decided to use some exerts from my favorite emergency physician/presenter, Dr. Amal Mattu. Dr. Mattu has spoke and written on these topics multiple times.

Bradycardia

This first one is easy, and you wouldn't even need a 12-lead to determine it's malignancy.

What do you notice about the 12-lead above? How about the rate? This is an example of bradycardia. Bradycardia may cause hypo-perfusion, leading to syncope. This would classify them as symptomatic, and they may require treatment.

*It is important to remember that there are many tachycardic arrhythmias that could cause syncope as well.

Acute Myocardial Infarction

An acute myocardial infarction (AMI) is the most common reason we use a 12-lead for diagnostic purposes. An AMI may cause syncope amongst many other signs and symptoms. Syncope would be an atypical (not usual) presentation for an AMI. I am not going to elaborate much on this presentation because it requires much teaching for those who are unfamiliar with STEMIs (ST-Elevated Myocardial Infarction). Please head over to the prehospital 12-lead blog for some great education on STEMIs.

Long QT Syndrome

Long QT Syndrome, or LQTS may lead to arrhythmias that lead to syncope. This happens due to something called an R on T phenomenon. The most common arrhythmia due to LQTS is Torsades de Pointes, however monomorphic ventricular tachycardia is possible. Syncope and/or seizures are common symptoms of the rhythms associated with LQTS.

Torsades de Pointes

From Dr. Amal Mattu:

Prolonged QT-Interval

• Prolonged QT-interval predisposes to torsades de pointes
• One of the key “can’t miss” diagnoses associated with syncope
• Perhaps a more common cause of syncope and sudden death than previously recognized?

Causes of QT-prolongation
• Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)
• Sodium channel blocking medications (many!)
• Includes Type IA medications, anticholinergics, cocaine, many antipsychotics, some antibiotics
• Acute myocardial ischemia (usually associated with inverted T-waves)
• CNS lesions, e.g. intracerebral hemorrhage (often associated with giant inverted T-waves)
• Hypothermia
• Congenital

How long is too long?
• QT-interval will vary based on patient’s heart rate
• Measure QT from beginning of the QRS complex to the end of the T-wave, and average over 3-5 beats
• “Corrected” QT-interval (Bazett formula): QTc = QT/√(RR)
• QTc is considered prolonged when > 450 msec in men and > 460 msec in women and children
• Major risk occurs in patients with QTc > 500 msec

Treatment
• Search for and correct underlying cause (e.g. correct electrolyte abnormalities, discontinue responsible medications, etc.)
• Congenital or idiopathic causes: beta-blocking medications attenuate adrenergic-mediated trigger mechanisms
• Treatment of torsades de pointes: cardioversion/defibrillation, magnesium if relatively stable (e.g. intermittent torsades): 2 grams IV over 2-3 minutes followed by infusion
• Overdrive pacing? Isoproterenol? Atropine? These are listed as possible treatments in acquired (not for congenital) cases, but rarely needed
• Post-conversion treatment with magnesium, not lidocaine/amiodarone/ procainamide! (unlike other forms of ventricular tachycardia); for congenital cases, add beta-blocking medications

Click here or here to learn about Long QT Syndrome

Brugada Syndrome

ECG example of Brugada Syndrome

Brugada syndrome is becoming more and more well known recently. It is associated with specific ECG changes and an increased risk for sudden cardiac arrest. Only known cause of Sudden Unexpected Death Syndrome (SUDS)--according to Wikipedia. The ECG changes associated with Brugada Syndrome are most visible in V1, and V2. Non-STEMI-like ST-elevation that cannot be explained by another pathological cause (ie. LVH, LBBB, BER) may be Brugada Syndrome. These individuals may be otherwise very healthy and/or young.

Some features of the different types of Brugada Syndrome include:

a RBBB pattern in V1 without terminal S-waves in lead I and V6.
A saddleback ST-elevation pattern (type 2 below)
Coved J-point elevation in V1, V2, V3 that gradually slopes down (type 1 below)

From Dr. Amal Mattu:

Brugada Syndrome

More common cause of sudden death than previously recognized
• May be responsible for up to 20% of sudden deaths in individuals without structural heart disease
• Responsible for 4-5% of all sudden deaths
• Incidence varies in different populations (some genetic factors involved)
• Most common in young males (< 50 yo.)
• First onset of symptoms approximately 40 yo.
• Mortality approximately 10% per year if not treated with an internal cardioverter-defibrillator (ICD), regardless of whether or not antiarrhythmics are used

Syndrome characterized by
• ECG abnormalities in leads V1 – V3
• Polymorphic or monomorphic (less common) ventricular tachycardia
• Causes syncope if self-terminating
• Causes sudden death if persists and not terminated by treatment
• Structurally normal heart
• Familial occurrence in approximately half of patients

ECG findings in leads V1 – V3
• Right bundle branch block (RBBB) or incomplete RBBB pattern
• ST-segment elevation — 2 types
• “coved-type” (most common)
• “saddle-type”
• ECG findings can vary with time depending on the autonomic balance, administration of antiarrhythmic and other drugs affecting channel function, body temperature, and other unknown factors

Definitive diagnosis can be made with electrophysiologic testing
• Challenge with an intravenous class I medication (e.g. ajmaline, procainamide, flecainide)
• Will induce increased ST-segment elevation and “coving”
• Programmed electrical stimulation of the heart
• Can induce ventricular tachycardia

Treatment
• Placement of an ICD is the only effective treatment
• Antiarrhythmic drugs (including beta blockers, amiodarone, etc.) ineffective

Click here or here for more on Brugada Syndrome

Hypertrophic Cardiomyopathy

From Dr. Amal Mattu:

Hypertrophic Cardiomyopathy (AKA IHSS, ASH, HOCM, etc.)

• Prevalence — 0.02% – 0.2% of the general population
• Genetic factors involved
• Hypertrophied but nondilated left ventricle
• Thickening is usually asymetric, involving the septum to a greater extent than the free ventricular wall
• Cardiomegaly usually not present on chest x-ray
• Mortality 3.5% per year
• Diagnosis often made only when the patient experiences sudden death
• Usually occurs during exertion \
• Average age at diagnosis is 30 – 40 yo.
• Patients may also experience syncope, angina, palpitations, dyspnea (often associated with exertion)

ECG findings
• Normal in 7% – 15%
• Typical abnormalities
• Deep narrow Q-waves in the inferior and/or lateral leads – I, aVL, V5-6 (simulates MI, but Q-waves are “too narrow” for MI)
• Very specific for this condition
• Q-waves in lateral leads are more common than inferior leads, very commonly misdiagnosed as lateral MI
• Left atrial enlargement
• High left ventricular voltage/left ventricular hypertrophy
• Other less common abnormalities
• Tall R-wave in lead V1 (simulates posterior MI)
• Deep narrow Q-waves in the inferior leads (simulates inferior MI)
• Don’t rely on your cardiologists to make the Dx on ECG! Clinical diagnosis
• Systolic murmur at apex or LLSB
• Murmur increases with valsalva, standing
• Murmur decreases with trendelenburg position, isometric exercise, squatting
• Definitive diagnosis — doppler echocardiography

Treatment
• Beta blockers, calcium channel blockers to improve LV filling and diastolic \function ]
• Amiodarone if ventricular dysrhythmias present

Unrecognized Killers in Emergency Electrocardiography

Amal Mattu, MD 7

Occupational Hazard: Playing the Fool

2010-06-08T03:04:00.010-04:00

Occupational Hazard: Playing the Fool is the title of a must read article by Michael W. Kahn, MD.

It starts out with an important question. Maybe this is a question that might be a good way to screen future health care workers - doctors, nurses, paramedics, et cetera.

“Can you tolerate being bamboozled by your patients from time to time?”^[1]

Maybe we should turn the question around.

Is it more important for us to punish some of our misbehaving patients, than to provide appropriate treatment to all of our patients?

Better to punish?

Better to treat?

This is the crux of one dialogue about appropriate pain management.

We deceive ourselves into believing that we can tell who is telling the truth and who is telling a lie. We base this belief on . . . ?

Well, what do we base this on?

Are there any studies that show how to identify the patient telling the truth?

or

Are there any studies that show how to identify the patient is not telling the truth?

Do we demand that our patients have an obvious extremity fracture, just to prove to us that they have pain worthy of treatment?

Why?

If the patient does not have some blatant injury, does that mean that there is no legitimate pain?

Why?

If the patient does not have some blatant injury, does that mean that their pain is not worthy of treatment?

Why?

That looks painful. You may have something for pain.

That doesn't look painful. You get Ultram.^*

I think we underemphasize the prevalence of certain normal errors inherent in medical practice. Surgeons are fooled when they open an acutely painful abdomen only to find a normal appendix: in the days before CT scans, it was said that if that didn’t happen once in a while, you weren’t operating often enough. When in doubt, it was safer (and wiser) to operate than to risk a rupture and peritonitis, even if the diagnosis was “wrong.” Here was an error that wasn’t an error, but rather a predictable side effect of balancing known risks with imperfect information.

I suggest that we apply a similar principle to the prescribing of narcotic painkillers and anti-anxiety drugs. Let’s assume that it’s impossible not to be fooled at least some of the time — that when assessing patients’ sincerity, we should expect a certain rate of false positives.^[1]

We have no ST scan to identify pain.

Since “first, do no harm” remains a guiding principle of care, let’s remember that the harm of missing a chance to help often greatly exceeds the harm of prescribing under a false pretext. Our system of justice is based on the idea that we should let the guilty go free rather than punish the innocent. Could our prescribing habits benefit from the same philosophy?^[1]

Go read the whole article.

Footnotes:

^ ¹ Occupational Hazard: Playing the Fool
by Michael W. Kahn, MD
New York Times.
Article

^ ^* Ultram
Wikipedia entry for tramadol.

Ultram is tramadol, which is just the result of another attempt to come up with a treatment for pain that is effective, but not addictive. The result is a drug that is addictive, but is not effective.

When I hear that a patient is receiving tramadol, it tells me that the doctor believes that the person is a drug seeker, but the doctor is afraid to refuse all pain medicine, so the doctor decides to give something they can document - Ultram.

Ultram = pain relief in documentation only.

.

Prehospital Stroke Care 2

2010-06-04T22:24:00.002-04:00

Cerebral Vascular Accident

Clot or Bleed?

By Adam Thompson, EMT-P

The stroke patient is one that is commonly seen and transported by EMS providers. There tends to be a frustration due to the inability to do much for these critically ill patients. Their quality of life subsides right before our eyes. There are two types of stroke as I explained in PART 1. There are treatments available for ischemic strokes that can tremendously benefit the patients if given soon enough. Thrombolytic therapy could be very effective in treating the ischemic stroke patient in the prehospital environment. The only problem is that if this treatment was used on a patient suffering from a hemorrhagic stroke, it could tremendously worsen that patient's condition. There is no way to conclusively differentiate between an ischemic or hemorrhagic stroke in the field without the use of diagnostic equipment. There are, however, many indicators that could clue you in on the probably etiology.

Risk factors for stroke

Most of the risk factors for stroke are the same for both subtypes. However, some are more indicative of a specific type. Knowing these may assist you, along with the presenting signs and symptoms.

More associated with ischemic stroke

Atrial fibrillation
History of TIAs
Increase in Vitamin K
Carotid artery disease
High cholesterol
Diabetes
Patent Foramen Ovale

More associated with hemorrhagic stroke

Severe acute hypertension
Anticoagulant medications
Smoking

Similar to risk factors, physical findings are not synonymous with a specific subtype, but they are very good indicators. These signs may indicate either type of stroke, I cannot stress that enough.

Signs of Hemorrhagic Stroke

Airway compromise
Complete unresponsiveness
Complete aphasia
Nausea & vomiting

Signs of Ischemic Stroke

Expressive aphasia
Unilateral deficits
Poor coordination

So it is possible to have a fairly good idea weather the stroke patient you are presented with is suffering from a clot or a bleed, based on a fine assessment. With advancements in technology, this skill, however, may eventually be unneeded. There is solid evidence supporting the efficacy of paramedics and the use of prehospital diagnostic equipment. There are portable brain scanners that are being tested in the field right now. This may sound like something far-fetched or unnecessary, but I believe otherwise. With stroke being the time is tissue condition, why not use equipment that may facilitate treatment that could subsequently improve the quality of life, of our patients. With the ability to conclusively diagnose an ischemic stroke, thrombolysis could be preformed much earlier. There would be an obvious need to provide research and gain evidence to support this process, but with an exponential probability of benefit, there should be a bigger push to get this done. The studies advocating hypothermia in the presence of a CVA all appear encouraging as well. Please read some of the research I have provided below.

Set up and run a thrombolysis service for acute stroke. [1]

Abstract

Intravenous thrombolysis significantly improves the chance of independent recovery from ischaemic stroke but its benefit is strongly time dependent: present evidence supports effectiveness when delivered up to 4.5 h after symptom onset but the chance of recovery is twice as great when it is given within 90 min compared with 3-4.5 h. Delivery of treatment to a high proportion of patients is possible but requires clinicians to optimise systems for patient transfer, clinical and radiological assessment. A high proportion of patients with stroke already present to UK hospitals within the treatment time window even without specific public awareness or prehospital triage. Establishing a service requires dialogue with all those involved in the patient pathway, including ambulance dispatchers, paramedics, emergency department staff, radiology and colleagues in acute medicine. Most acute stroke teams cross traditional medical disciplines. Thrombolysis should ideally be delivered within an integrated service that seamlessly includes acute stroke unit care and rehabilitation.

Transcranial ultrasound from diagnosis to early stroke treatment. 1. Feasibility of prehospital cerebrovascular assessment. [2]

Abstract

BACKGROUND: To test whether portable duplex ultrasound devices can be used in a prehospital '911' emergency situation to assess intracranial arteries. METHODS: Non-contrast-enhanced transcranial duplex ultrasound studies were performed either immediately at the site of the emergency (i.e. private home) or after transfer into the emergency helicopter/ambulance vehicle. RESULTS: A total of 25 patients were enrolled. In 5/25 cases, intracranial vessels could not be visualized due to insufficient quality of the temporal bone window. In 20/25 cases, bilateral visualization and Doppler flow measurements of the middle cerebral artery could be assessed in a mean time less than 2 min. CONCLUSION: Emergency assessment of intracranial arteries using portable duplex ultrasound devices is feasible shortly after arrival at the patient's site. 2008 S. Karger AG, Basel.

A noninvasive portable acoustic diagnostic system to differentiate ischemic from hemorrhagic stroke. [3]

Abstract

PURPOSE: To determine if a noninvasive brain acoustic monitor can differentiate acoustic responses from "normal patients" and ischemic from hemorrhagic stroke patients. METHODS: A laptop-sized passive acoustic monitoring system acquires arterial-pressure-generated signals during a 15-second monitoring session from sensors placed at the radial artery and on the fore-head. The arterial pulse waveform from the head is compared with that of the arterial waveform to generate the time-domain signal comparison. Frequency domain signals from each area are also compared. The study involved patients with diagnosis of first stroke who could be monitored within 12 hours of symptom onset and normal subjects who provided informed consent. Individuals with history of brain injury, stroke, or other brain disease were excluded. RESULTS: Twelve normal subjects and 6 ischemic stroke, 2 transient ischemic attack (TIA), and 3 hemorrhagic stroke patients were monitored. Frequency response analysis identified uniform frequency responses in normal subjects. The signal in ischemic stroke patients was characterized by a divergence of the radial and cranial frequency response between 10 and 50 Hz of 10 dB or greater. In intracerebral hemorrhage patients, a divergence was seen below 10 Hz but not in the band above 10 Hz. TIA patients were monitored after symptom resolution and showed a divergence <10 dB in both bands, similar to normal subjects. CONCLUSIONS: In a pilot study using a noninvasive monitor, the authors detected a potential to differentiate between normal subjects and those with cerebral ischemia or hemorrhage.

Comparison of neuroprotective effects in ischemic rats with different hypothermia procedures. [4]

Abstract

OBJECTIVE: The neuroprotective effect of hypothermia has long been recognized. The aim of this work was to compare the neuroprotective effect of systemic, head and local vascular cooling hypothermia procedures in ischemic rats. METHODS: Stroke in Sprague-Dawley rats (n=64) was induced by a 3 hour right middle cerebral artery occlusion using an intraluminal filament. Before reperfusion, ischemic animals (n=16 in each group) received hypothermia (systemic, head or local vascular) or no treatment. Brain temperature, infarction volume (n=8 in each group) and functional outcome (n=8 in each group) were compared. RESULTS: Regarding brain temperature, vascular cooling significantly reduced the temperature of ischemic territory in cortex from 37.2 +/- 0.1 to 33.4 +/- 0.4 degrees C and in striatum from 37.5 +/- 0.2 to 33.9 +/- 0.4 degrees C within 5 minutes. This hypothermic condition remained for up to 60 minutes after reperfusion. However, systemic cooling reduced brain temperature at a similar level for six times longer. In the head cooling group, the target temperature was reached in 15 minutes, but returned to normal within 5 minutes. Although all hypothermia procedures induced neuroprotection, ischemic rats with vascular cooling showed significantly (p<0.001) better neuroprotection with 10.7 +/- 2.6% infarction, compared to 54.2 +/- 1.9% (no treatment), 37.1 +/- 1.0% (head cooling) and 29.1 +/- 3.4% (systemic cooling). Significantly (p<0.001) better effects on motor function were also detected in vascular cooling groups at 14 and 28 days. CONCLUSION: Vascular cooling appears to be the most effective in reducing infarct volume and improving functional outcome than the other two hypothermia methods in a rat ischemia/reperfusion model.

A protocol to improve analgesia use in the accident and emergency department

2010-06-04T04:25:00.011-04:00

Last month I pointed out Prehospital use of analgesia for suspected extremity fractures. The study I am covering now looks at a similar group of patients in A&E (Accident & Emergency - the British version of ED - Emergency Department).

We aimed to assess the use of analgesia within our department and identify shortcomings. Having done this we devised a protocol for intervention and assessed whether this was successful. We chose acute skeletal injuries as a well defined group of unequivocally painful injuries that could readily be assessed.^[1]

The authors don't even doubt that they have a problem. They already have a plan to fix the problem. They claim that they are looking at a well defined group of unequivocally painful injuries that could readily be assessed. Not all fractures cause moderate to severe pain. Using opioids for minor pain, even if from a fracture, is not good medicine. Even their results do not agree. The doctors in this study do seem to have been equivocal, when it came to the pain of their patients.

Methods
One hundred consecutive referrals to the fracture clinic and 100 orthopaedic admissions were analysed for the following data: (1) patient's sex and age; (2) injury sustained; (3) analgesia given in A&E department: drug used, dosage, route of administration.^[1]

Using consecutive referrals is a good way to randomize to avoid selection bias. This is one of the things that Ex-Dr. Andrew Wakefield did that was a reason for eventually retracting his autistic enterocolitis paper, although it was just one of many problems with that paper.

The results of this audit were presented at a staff meeting. An analgesic protocol (figure) was then introduced and circulated through the department to all staff.^[1]

Here is the protocol they came up with.

The Notes at the bottom are interesting.

1. Act on clinical suspicion - do not wait for x rays.^[1]

This is nice and logical.

An x ray does not tell you anything about the pain the patient is experiencing. Waiting for an x ray does nothing to help the patient. If anything, trying to position a painful injury for x ray, will probably increase the patient's pain and is likely to make it more difficult to obtain a clear x ray.

Waiting for an x ray makes as much sense as delaying treatment of abdominal pain until after the patient is assessed by a surgeon. There is no evidence to support either excuse for delaying pain management.

2. Use Entonox during assessment.^[1]

Entonox is a brand of nitrous oxide/oxygen mixture. This can decrease the amount of opioid needed to appropriately manage the patient's pain. Since the goal is pain management, not opioid dose, this is a good thing.

One huge confounder is the complete lack of mention of nitrous oxide anywhere else in the study.

Did all patients receive nitrous oxide?

What about before the study?

If they have been using nitrous oxide and using it aggressively, then their pain management is better than it appears, but why is there no other mention of nitrous oxide. They mention paracetamol, which is the Commonwealth name for acetaminophen, (commonly sold under the brand name of Tylenol), but ignore any mention of nitrous oxide? Nitrous oxide can be an excellent pain medication. Nitrous oxide is not used enough. In this study, we don't know if it was used at all, even though we are presented with a protocol stating Use Entonox during assessment.

3. All opiates must be given with an IV anti-emetic in adult patients.^[1]

This could generate a couple of blog posts on its own.

The preferred route of administration for titratable medication is IV (IntraVenous). The use of IM (IntraMuscular) opiate is not a good idea. IM use may be based on a combination of ignorance and being too lazy to start an IV, although the authors suggest that this is a vascular access problem. Maybe.

Why would someone use IV anti-emetic medication in combination with IM pain medication? Given IM, the effect is delayed. Given IM, the ability to titrate is compromised. Given IM, much more medication is required to produce the same effect.

There is rarely a need for anti-emetic medication when treating patients with opioid medications - even with large doses of opioids. It is important to not give the medication as a fast push. Almost all of the adverse effects/side effects are rate/dose related. Either the rate of administration increases the frequency of the side effect, or the total increases the frequency of the side effect, or both. The rate may be most likely to induce side effects during the first dose of a medication, while the total dose may be more likely to produce side effects with the later doses.

An anti-emetic generally produces sedative effects. If we want to sedate the patient, midazolam may be a more appropriate choice.

If nausea is present, I find that morphine or fentanyl will do a great job of decreasing the nausea by decreasing the pain that appears to be causing the nausea.

In one of the Star Wars movies, Yoda explain a problem with fear. However, Yoda does not point out the obvious. Fear also has an origin. Fear is often due to ignorance.

“Fear is the path to the dark side. Fear leads to anger. Anger leads to hate. Hate leads to suffering.”

Yoda also stops with suffering, but even suffering is not the worst of it. I would write it this way -

Ignorance is the path to abuse. Ignorance leads to fear. Fear leads to denial. Denial leads to suffering. Suffering leads to self-delusion. Self-delusion leads to complacency.

When we see the suffering we have increased, we delude ourselves about the actual cause of that suffering. We pretend that we are really acting in the best interest of the patient, but aren't we really acting to protect our ignorance?

Self-delusion is what allows us to make up all sorts of excuses for abuse. Once we start deluding ourselves, where do we stop?

Once we start deluding ourselves, do we maintain any reason to examine what we do?

Their pain isn't that bad.

I know a faker when I see one.

Pain builds character.

We don't want to turn them into addicts.

It's a slippery slope.

Once we start treating one patient's pain, we will be invaded by hordes of drug seekers faking hip fractures, tib/fib fractures, humerus fractures, third degree burns, et cetera.

That doesn't hurt.

These drugs are dangerous.

Fentanyl is much too potent.

Respiratory depression will sneak up on the patient and carry the patient off to the morgue before anyone can notice.

It's for your own good.

Man up.

What if . . . ?

The use of these phrases indicates ignorance about the appropriate use of opioid medications.

We should not let the Jenny McCarthys of pain management guide our treatment decisions. We should be educating the ignorant, so that they better understand pain management.

Ignorance is only a problem if it is maintained. We are all ignorant, just on different subjects.

How we deal with our ignorance determines how we treat our patients.

Act on clinical suspicion - do not wait for x rays.^[1]

There is a big problem with this study and the previous study I wrote about. They only look at fractures. They do not look at pain. They do not measure pain. They use the fracture as a surrogate for pain. Fractures often are painful.

What does an x ray tell you about the patient's pain?

Not a thing.

The x ray will tell you something about what appears to be causing the pain, but opioids are not a part of the treatment of fractures. Opioids are a part of the treatment of pain.

If the pain is not due to a fracture, but is due to a sprain, or a strain, or a tumor, or an insect bite, or a poisoning, or an embolus, or a burn, or ischemia, or any of the many other causes of pain - should we ignore that pain just because there is no fracture?

No.

We should not ignore pain until after an x ray.

We should not ignore pain until after arrival at the hospital.

We should not ignore pain until after transport.

We should not ignore pain until after immobilization.

We should treat the pain as soon as is appropriate.

If I have a patient with an apparent hip fracture - painful deformity to a leg that appears shortened and externally rotated - I only need to know a little bit of information before initiating treatment. A quick assessment (including circulation, sensation, and movement distal to the injury, vital signs, and pain rating), a list of allergies and medications, and a history. This takes a couple of minutes. I also need IV access. This may take another couple of minutes. Then it is all a matter of give a bit of fentanyl and reassess, repeating every 5 minutes, until the pain is reduced to a level, where it is appropriate to move the patient.

If it takes 10 minutes to manage the pain, that is not a problem.

If it takes half an hour to manage the pain, that is not a problem.

If it takes over an hour to manage the pain, that is not a problem.

These are only problems if we are more worried about our hypothetical next patient than we are worried about our current patient. I am able to provide a significant benefit to this patient, but some people are more interested in some other patient who might benefit more. If we are going to be treating patients, we need to act as if we have the maturity to pay attention to the current patient, not dreaming about other patients with potentially greater life threats.

What if . . . ?

What if we actually provide competent care, rather than worry about the things that are not happening?

What if we really do have other ambulances and mutual aid agreements to deal with more than one call at a time?

What if we have exaggerated the importance of response times beyond what is remotely reasonable?

Over the following one month a further 100 consecutive referrals to fracture clinic and 100 orthopaedic admissions were then assessed using the same criteria.^[1]

One nice thing about this is that it makes the percentages of the total easy to work with. 1 = 1%. There were 100 patients in each of the original groups, so it is easy to compare. That is a total of 400 patients, but it would be better with a lot more patients.

Results

FRACTURE CLINIC REFERRALS
These were divided into four groups: forearm, lower leg/ankle, hand/foot, and others. The numbers of fractures assessed in the initial and repeat audit are shown in table 1. The analgesia given is detailed in table 2. Fracture clinic referrals receiving unsatisfactory analgesia were reduced from 91 % to 69%, a difference of 22% (95% confidence interval 10.9% to 33.1%, P < 0.001).^[1]

Let's look at that a little bit differently. If 91% of these patients are receiving unsatisfactory analgesia, then we might conclude that 9% of patients are receiving satisfactory analgesia. After the protocol, this increases to 31%. They describe this as a 22% improvement.

If they were trying to increase sales of a drug, would they be reporting these numbers this way? If a competing drug showed an effect in 3% of patients, and the drug being studied showed an effect in 6% of patients, would the advertisements claim 3% more effective than our competitor? No, they would not. The drug would have doubled the effect. Whether that doubling is relevant depends on a lot of things. The ads would probably claim 100% more effective than our competitor or, the same information expressed for a different effect, 200% as effective as our competitor.

The increase in patients receiving satisfactory analgesia increases from 9% to 31% an increase of 22% of the total number of patients, but an increase of 244% above the original 9%. 22 is almost 2 1/2 times 9.

There are several things to mention about this.

91% unsatisfactory is pretty bad. The authors acknowledged that they were not happy with that. They sought to improve things. The improvement was dramatic.

Imagine if you are back in grade school and you get a score of 9% on a test. We will assume that this was not a grade on a multiple choice test, because unless there were an average of eleven choices for each question, you would be expected to do better by just guessing.

If you have a 9% score on your first test, but get 31% on the next test, are you going to be bragging to your parents? No, you probably are not. It is more likely that you will be offering to get the mail every day for a while. You may be engaging in a bit of triage of mail from the school, or hacking the parents' email to redirect school emails to you.

65% is the minimum score to be considered passing in many places. If you took 31% and doubled it, you still would not receive a passing score. Can you claim that you have learned 244% more between Test 1 and Test 2? That may depend on how little you knew at the time of Test 1.

There is no Limitations section, so I created a sample of what that might include.

What is not reported in this study:

Was there any change in availability of opioids?

Was there any change in supplier of opioids?

Was there any change in requirements for documentation?

Had there been any event before the first part of this study that had staff especially worried about pain management, a worry that might have eased with time?

Were there any incentives offered with the introduction of the new protocol?

Was there anything done to track longer term changes in treatment?

Was there any change in the staffing (different hours, new hires, vacation coverage, et cetera)?

Were there any other changes to the way that the patients were treated?

As you can see, there are many things that are not described as being controlled for in the study. Therefore, we should not presume that any of them have been controlled for. What is the confidence interval based on? Just statistics, or is there some understanding of the potential variables? Since this is an early pain management study, I do not expect that there is the kind of awareness of the relevant variables that the same authors would have today.

How sad is it that a study of pain management published in 1996 is considered early?

What did we base our treatment on before then? Unfortunately, we based our treatment on a lot of misinformation. We still do this, but we are getting better at pointing out the misinformation and correcting those spreading misinformation.

That was the Fracture Clinic. Initially, 91% of patients did not receive any medication for their fractures. None of those patients declined pain medicine.

Since I am writing mostly about opioid medication for pain management, I should mention that in the first part, the number of patients receiving opioids is zero IM and zero IV. 4 patients received paracetamol. A whopping 4 patients received this aggressive treatment. They could have done just as well by going to their medicine cabinet and taking their own over-the-counter medicine.

In the second part, those numbers zoom all the way up to IM opioids = 3 and IV opioids = 3. This is not impressive. This is just something is better than nothing.

For those in America, reading this and saying to yourself, I'm just glad I am in America.

Do you really think that pain management is/was better in America?

If you do think pain management is/was better in America, what do you base that on?

ORTHOPAEDIC ADMISSIONS
These were also divided into four groups: neck of femur, forearm, lower leg/ankle, and others. The numbers of fractures assessed are given in table 3 and the analgesics used in table 4. Orthopaedic admissions receiving unsatisfactory analgesia were reduced from 39% to 22%, a fall of 17% (95% confidence interval 4.2% to 29.8%, P = 0.009). The number of orthopaedic admissions receiving intravenous opiates increased by 28%, from 9% to 37% (95% confidence interval 16.3% to 39.7%, P < 0.001). The most appreciable improvements in analgesia used were obtained treating patients with fractured neck of femur (table 5).^[1]

Orthopaedic admissions receiving unsatisfactory analgesia were reduced from 39% to 22% It is great that we are dealing with numbers that are much higher in this group. Still, this implies that only 61% rated their pain management as acceptable. That improved to 78% after the introduction of their protocol.

Intravenous analgesia is superior to intramuscular analgesia for reasons of speed of onset, reliability of uptake, and the ability to titrate doses to response.^{4 6} The number of orthopaedic admissions receiving intravenous opiates increased by 28% following the introduction of the protocol.^[1]

I have no argument with the reasoning, but they should have already been aware of that before the start of the study. Just as they already should have been aware of this little tidbit - Pain Hurts.

We were particularly successful in improving analgesia for patients with fractured neck of femur. Perhaps the value of intravenous titration of doses is better appreciated in the elderly population who typically suffer this injury.^[1]

I would reword that, but I don't think that I am really changing their meaning.

Perhaps the doctors in this study are more comfortable using intravenous titration of doses to better manage the pain in the elderly population who typically suffer this injury (hip fracture).

And by better I mean more safely and with fewer side effects and with faster onset and with a more accurate end point.

This was from the dark ages of pain management, which was only 14 years ago where this study was done. Other places may not have progressed beyond this point, even now. It is good that the authors looked at their practices. I expect that they are much more aggressive today than what is shown in this study.

And for the punchline we have this -

Setting- University teaching hospital.^[1]

These are supposed to be doctors with the most education, the most resources, the most experience, et cetera. These are supposed to be the doctors who are educating the doctors of the next generation. Even in an academic medical center, they appear to have been held back by the mythology of pain medicine, but they are changing that mythology.

Discussion
The management of pain in acute trauma is often neglected.^{1 2} Patients arriving at A&E departments with acute trauma are unlikely to have received sufficient analgesia,³ so responsibility lies with the attending doctor.^[1]

Sometimes the best way to encourage the doctors to treat pain appropriately is to authorize EMS to treat pain appropriately. Doctors are capable of both compassion and learning, but sometimes they do seem to need a push. The authors of this study did provide a bit of a push. Did things continue to progress, or did they revert to whatever was the mean at this A&E?

Footnotes:

^ ¹ A protocol to improve analgesia use in the accident and emergency department.
Goodacre SW, Roden RK.
J Accid Emerg Med. 1996 May;13(3):177-9.
PMID: 8733653 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central

Free Full Text PDF from PubMed Central

.

S.A.L.T. Device

2010-05-30T14:21:00.004-04:00

Supraglottic Airway Laryngopharyngeal Tube

Link to product: S.A.L.T.

Some videos:

I have used the S.A.L.T. device once on a cardiac arrest patient. Initially it found it's way in the right mainstem bronchus; which we easily resolved. Others have told me that they have had problems with the securing device. Some have stated that they have had trouble avoiding esophageal placement. I am not certain if the S.A.L.T. device will replace the King LT as my choice for cardiac arrest victims, but it is an interesting product nonetheless. It may have it's place in primary respiratory arrest. I am still a fan of videolaryngoscopy at the moment, even if it is the most expensive option.

66 year old male CC: Chest pain

2010-05-29T13:09:00.002-04:00

Here's another great case submitted by Nick Ciaravella of Grady EMS in Atlanta, GA.

66 year old male presents to EMS with chest pain.

S - Chest Pain
A - None
M - Atenolol, HCTZ
P - HTN
L - meal, 7 hours prior to event
E - Mowing his lawn

O - Started while mowing his lawn
P - Provoked while exerting himself, Palliated initially when he sat down to rest
Q - Sharp
R - Substernal, initially radiating to his jaw, when he rested the pain was only in his chest
S - Initially 10/10, upon ems arrival 4/10, en route 8/10, 9/10, and 10/10 upon arrival at ED
T - No previous episodes

The patient initially presented to EMS with 4/10 pain and vitals as follows, 148/84, pulse 72, 18 respirations, SPO2 96%, Lung sounds clear and equal, BGL 103.

The patient was placed on 3 LPM O2 via NC, given 324 mg Aspirin PO, given 0.4 mg Nitro Tablet Sublingual and then 1 inch of Nitro Paste Transdermal. The Patients pain increased en route to the ED and began to radiate down his left arm en route.

12-lead ECG #1

12-lead ECG #2 (about 15 minutes later)

What do you think?

See also:

Anterior ischemia or posterior STEMI?

26 year old male CC: Chest pain

74 year old male CC: Chest pain

50 year old male CC: Respiratory distress, chest pain

48 year old male CC: Chest discomfort, shortness of breath

Pure (Isolated) Posterior STEMI -- not so rare, but often ignored! - Dr. Smith's ECG Blog

Empathetic vs. Pathetic

2010-05-27T20:33:00.007-04:00

Empathetic vs. Pathetic

Listen up EMS

By Adam Thompson, EMT-P

I know I have pretty much kept this blog purely aimed towards education, fact, and evidence. It is time for a rant though.

Please read the following links before continuing:

So what do we do? How do we change the attitude of our fellow EMSers? Do we need to make the change, or do they?

This is something I have been cognizant of for some time. Being an overachiever in EMS gains you no friends. The more successful you are, the bigger your blip is on the radar of ridicule. But who cares, right? They aren't talking about you for being a cretin medic that screws up on calls.

Example. I am a young, but experienced medic. I have achieved a lot in my career. I am a published author. My training captain recently sent out one of my articles with a thumbs up message to my entire agency. The response was as good as it was bad. The ongoing joke is with every conversation I bring up I hear "why don't you go write an article about it". Some of this may be just a joke, but I can feel the animosity from many. Why?

The Problem

I think, from my experience I have pinned down one problem. We are our own bosses.

I know we all have bosses, chiefs, supervisors, what have you. What I mean is, most of us don't have those people on our trucks with us. If you work in a system like mine, you may be the lone medic working with an EMT, or maybe you are the EMT. I think that the systems that have multiple medics per ambulance suffer less from these issues--and here's why.

If you are use to making your own decisions with little repercussion and the ignorant feeling of correct-fulness, you will not likely be inclined to take advice from your fellow medics. I dread the response of a peer that I attempt to assist with a smidgen of education. Because there is a naive belief that they know EVERYTHING.

Why are we so damn sensitive?

If you haven't read my letter to the new guy, go read it. It is time we toughen up. If a salesman isn't making a company any money, are the bosses going to be fearful to approach him?

I was speaking with one of the white shirts (officer) from the training department the other day and made some proposals. I said we should have a real QI/QA committee that picks ten calls at random every month. Some ran good, some not so good. Then, the medics on each of those calls would have to present each case in front of their peers. There would be questions and answers.

My thought was that we hear about the bad calls through hearsay all the time, but do those medics get to defend themselves on a normal basis--no! A lot gets lost in translation. Sometimes you have to be on a call to understand, right? Well here is the chance to remedy that while implementing a QI/QA process that physicians use and grow from.

His response: The union will never allow it.

What the hell are we doing to ourselves? While unions might be established to protect the best employees, why do they work so hard to keep the worst? We can learn so much from each other, but you can't learn if you keep thinking there is nothing left to learn.

We all mess up. Get over it!

I consider myself a pretty educated paramedic. I have made many mistakes.

Now think about that. When do you learn most? I'm not saying that there is a cemetery somewhere, filled with all my mess-ups. I'm talking about simple, little mistakes. Mistakes that if unmade, would have lead to more information and a faster diagnosis or better treatment modality.

If you think you are invincible, go ahead and continue living on your beachfront desert property. You make mistakes too.

If you can learn so much from your mistakes, and I can learn so much from mine, why can't we BOTH learn from EACH OTHER'S mistakes? This of coarse requires a deflation of bulbous craniums.

When did this stop being about the patients?

Empathy is a virtue that is quickly finding itself on the endangered attributes list.

Please read Professionalism: What we say by me.

No matter what you read here, or believe. No matter how long you have been doing this. No matter how bitter you are. You have to agree that at some point of your career you wanted to help people. You wanted to make a difference, and do some good. So I ask you this... Are you?

PowerPoint Presentation on Strain Patterns!

2010-05-22T18:23:00.005-04:00

This is an awesome PowerPoint presentation from one of my favorite ECG textbooks, 12-Lead ECG - The Art of Interpretation.

You owe it to yourself to purchase this book (and no, they don't pay me to say that).

Make sure you use "full screen" so you can see all of the features of this important presentation. Pay special attention to slides 33-47!

Slide 45 shows a strain pattern from left ventricular hypertrophy (LVH).

Slide 47 shows a split screen with a strain pattern from right ventricular hypertrophy (RVH) on the left and acute infero-posterior STEMI on the right.

This is the book that taught me how to recognize strain patterns! So pay attention because this is one of the most important STEMI mimics!

Chapter14

See more presentations by rsprue1 | Upload your own PowerPoint presentations

Comment on Intravenous morphine at 0.1 mg/kg is not effective for controlling severe acute pain in the majority of patients

2010-05-20T06:35:00.002-04:00

In response to Intravenous morphine at 0.1 mg/kg is not effective for controlling severe acute pain in the majority of patients, there is a comment by medic.

thank you for your post. i'd like to add a few thoughts, and please feel free to comment on them.

Thank you.

1. i have a suspicion that pts who rate their pain 7-8/10 tend to be more honest about their pain than the ones who rate their pain 10/10 (worst pain ever), which perhaps partially explains the study's findings when sorted by initial pain rating.

That may be. Pain is subjective. Out of 119 patients, only 5 rated their pain 7 out of 10, so this is a small fraction that may not indicate anything. If we wish to draw conclusions about patients with 7 out of 10 pain, we need to set up a much larger study and propose our hypotheses before the study is begun.

Even if a report of 7 out of 10 pain is more honest than a report of 10 out of 10 pain, does that make it any less appropriate to treat 10 out of 10 pain aggressively?

2. competence is a huge factor is any setting, not just ems. there are plenty of (supposedly better-trained) docs and nurses who are clearly retarded.

Retarded is not the right word. However many doctors, nurses, and medics just do not get it. Maybe pain management has not been explained to them in the right way.

Many doctors do seem to become much more comfortable using opioids to treat pain after experiencing severe pain themselves.

We never seem to hear about doctors becoming less comfortable using opioids after experiencing severe pain.

This suggests that there is something important that is not understood by the doctors until after experiencing severe pain.

I suspect that studying this might require a huge sample of doctors, just to be able to track the change in prescribing/ordering habits vs. personal experience of severe pain, whether their own pain or the pain of someone they care deeply about.

3. i personally have a high threshold for when i break the narcs open, as i too work in a poor area. that's not to say poor people can't have pain; that's just taking into account other factors such as a seemingly higher rate of drug use/abuse.

It isn't our pain threshold that matters, but the patients' pain threshold.

Opioids are not the appropriate treatment for all pain, but it is appropriate to treat severe pain aggressively with opioids when nothing else works (such as when nothing else is available). Nitrous oxide is something that can be safely used that might significantly decrease the amount of morphine needed to manage severe pain.

4. once i make the decision to use narcs, i am not stingy with them as experience shows that prehospital morphine doses are clearly inadequate. the more important issue here is a training crews for a heightened awareness of the potential for respiratory depression and allergic reactions (just had one last week).

And what did you need to do for the allergic reaction? Diphenhydramine?

Just because something happened last week, does not mean that it is common. We need to be aware of the potential for allergic reactions with all of our medications.

One of the many advantages of fentanyl, over morphine, is that fentanyl is much less likely to produce an allergic reaction.

Recognizing and dealing with respiratory depression should not require anything more than competently monitoring the patient.

Many, but not all, patients will experience respiratory depression with appropriate pain management, because pain tends to stimulate a sympathetic response. Having respirations decrease to normal is a good thing, even though this is respiratory depression.

If the patient shows signs of inadequate oxygenation/ventillation due to respiratory depression, then all that needs to be done is to get the patient to talk. Find a subject that the patient is interested in, people love to talk about themselves, and get them to keep talking. Or just keep asking questions that are not answered with a nod, or shake, of the head. Ask orientation questions. Even just telling the patient to take a deep breath every so often will work.

A talking patient is a breathing patient.

5. it's a big training issue to get crews to recognize those pts who are in pain and those who are trying to score narcs. this is where experience counts and it's difficult to teach. that being said, it's risky to presume that people are trying to score narcs.

We should not presume that people are trying to manipulate us to give them drugs inappropriately. We should be aggressively looking for indications that the patient has legitimate pain.

If I need to give out morphine and fentanyl to a bunch of junkies in order to avoid missing some patients with legitimate pain, then I will be the candy man.

Let me put this in perspective.

If I need to give out albuterol nebulizer treatments to a bunch of people who do not need nebulizer treatments in order to avoid missing some patients with legitimate asthma/emphysema/bronchitis, then I will be the nebulizer man.

If I need to give out IV dextrose to a bunch of people who do not need to receive dextrose through an IV in order to avoid missing some patients with legitimate hypoglycemia and an inability to take glucose by mouth, then I will be the dextrose infusion man.

If I need to take some people with minor injuries to a trauma center in order to avoid missing some critical trauma patients, then I will be the minor trauma man.

I am not encouraging over-treatment, for the sake of over-treatment. We do need to be much better at assessment, rather than treating mechanism. How much training do we have at recognizing drug seekers, who are not seeking drugs for legitimate pain? If we are trained at this in paramedic school, or on the job, what are the qualifications of the person providing this training? What research has been done to demonstrate the accuracy of the methods of differentiating between legitimate drug seekers and illegitimate drug seekers?

The best way to make someone a drug seeker may be to under-treat their pain.

Our concern needs to be much less on being police and much more on being paramedics.

.

62 year old male CC: Chest pain

2010-05-19T16:46:00.001-04:00

62 year old male presents to the emergency department complaining of chest discomfort.

Past medical history is significant for dyslipidemia and ulcerative colitis. Also prior history of significant tobacco use. Maternal history of CAD. Maternal and paternal history of CVA.

The patient's only medication is Lipitor but he took an aspinin en route to the hospital.

Onset: Patient states the pain started that morning and became progressively worse since lunch time.

Provoke: Nothing makes the pain better or worse.

Quality: Sharp and nonpleuritic

Radiate: The pain radiates down the right arm to the bicep.

Severity: 7/10

Time: Patient states he experienced a similar pain in his right upper chest several days prior while playing tennis. He stopped exercising and the pain resolved.

The pain makes the patient feel "a little clammy." He denies shortness of breath. He states that he feels "a little dizzy" but denies palpitations. He had a negative stress test 3-4 years ago.

He has a known history of left bundle branch block.

The patient's skin is warm and dry.

Breath sounds clear bilaterally. No JVD.

Neuro exam normal.

Vital signs:

Resp: 18

Pulse: 60

BP: 140/72

SpO2: 98 on RA

A 12-lead ECG is captured and presented to the ED physician within 5 minutes of arrival.

An "old" ECG is pulled from the computer system for comparison.

What is your impression?

** Update 05/19/2010 **

After oxygen and nitroglycerin the patient reports a significant decrease in pain.

An additional 12-lead ECG is captured.

There is now slightly less ST-elevation in leads V3 and V4.

Remember that a secondary ST-segment abnormality (as opposed to a primary ST-segment abnormality) should not "improve" with oxygen and nitroglycerin!

In other words, if this ST-elevation was caused just by the LBBB, it shouldn't be "getting better". Changing ST-segments suggest the dynamic supply vs. demand characteristics of ACS!

Now, let's go back to the initial 12-lead ECG. Is the ST-elevation in the anterior leads cause for concern?

Go back and read Identifying AMI in the presence of left bundle branch block (or paced rhythm). Remember, discordant ST-elevation = or > 5 mm is the least specific of Sgarbossa's criteria! That's why we use the modified rule that I learned from Dr. Stephen Smith of Dr. Smith's ECG Blog.

That criterion states that discordant ST-elevation should not be more than 0.2 (or 20%) the depth of the S-wave in the setting of left bundle branch block (ST/S ratio).

Using that criterion, how does this ECG measure up? Let's take a look.

Ladies and gentlemen, we have a winner!

The patient was ultimately cathed and angiography revealed 100% occlusion of the LAD.

Final thought:

Does it get any more difficult that that? If Dr. Smith's decision rule works this great, shouldn't we be shouting it from the rooftops?

See also:

Discordant ST-elevation in LBBB or paced rhythm

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graph

"New" LBBB - What's the big deal?

New left bundle branch block is a poor indicator of coronary occlusion - Dr. Smith's ECG Blog

STEMI best seen in PVC (Dr. Smith's ECG Blog)

Prehospital use of analgesia for suspected extremity fractures

2010-05-18T01:47:00.003-04:00

This is an older study that puts the prehospital pain management problem into a bit of perspective. While prehospital pain management has improved a lot in some places, other places may still be handling pain as described in this study. This is only ten years old. Attitudes are not changed so easily.

The authors looked at what is probably the least controversial type of pain management. If you were to ask medical directors what they feel most comfortable having paramedics use opioids to treat, the only other choice is likelty to be pain due to burns. Chest pain became a bit controversial after the CRUSADE study, but I will get to that in another post.

Over the last decade, pain and its management have received considerable attention. Most notably members of the medical profession in general and specifically emergency medical professionals undertreat pain to a considerable extent.³^[1]

While I would love to be able to defend everyone from this charge euphemistically referred to as undertreatment, the reality is that a decade later, the problem has not changed that much.

This was an observational study involving a retrospective review of all emergency medical services (EMS) runs for suspected extremity fractures^[1]

During the study period, all EMS run reports were evaluated by the fire department’s quality assurance coordinator. Only reports documenting the paramedic’s impression that the patient had sustained a fracture, or suspected fracture, of any extremity were included in the database.^[1]

There is no mention of any requirement to document any kind of measurement of pain. This seems to be the most significant problem with pain management in the system studied. How do we assess the quality of pain management if we do not assess pain?

The whole structure of this study revolves around the apparent inability to assess pain. There are a bunch of conclusions drawn. Here is what may be the most important omission of the study.

If we do not assess something, how do we treat it appropriately?

If a medical director does not make it clear that pain assessment and management are taken seriously, then is there much reason to expect the paramedics to be more aggressive than the medical director?

We need to provoke medical directors, emergency physicians, emergency nurses, EMTs, and paramedics to take pain seriously.

It's not my pain.

Akron Fire EMS employs a two-tiered transport system whereby nonurgent patients who may be safely transported in a private vehicle are deemed code 1, allowing the med unit to be put back into service. Nonurgent patients who require ambulance transport to the hospital become code 2 and their care and transport to the hospital are transferred to a private ambulance. A patient requiring immediate transport, medication, or procedures rendered by a paramedic is transported directly to the hospital as a code 3.^[1]

The two-tiered structure of this EMS system may unwittingly serve to negatively affect the administration of pain medication in several ways. Administering pain medication to a code 2 patient, for whom transport to the emergency department would be transferred to a private ambulance, would automatically change the run to a code 3. Upgrade to a code 3 would necessitate transport directly to the emergency department by the treating paramedic squad, extending the time required to complete the run.^[1]

Another question is whether code 3 means a lights and sirens transport to the ED. What extremity fractures, other than those cutting off circulation, require such rapid and rough transport? Even fractures cutting off circulation are unlikely to benefit from the slight difference in transport time that lights and sirens would provide. Slightly faster, but much rougher and much more painful in spite of the pain medicine! Why?

How did this service do at using pain medicine to manage suspected extremity fractures, which are expected to have a high correlation with severe pain?

A total of 18 patients (1.8%) received treatment for pain; nitrous oxide was administered to 16 patients (1.6%), and morphine sulfate to two patients (0.2%).^[1]

We know that 16 patients (out of a thousand patients with suspected extremity fractures) received nitrous oxide and 2 patients (out of a thousand patients with suspected extremity fractures) received morphine.

We do not know if they were being treated for pain, since there is no indication of any assessment of pain. We expect that the patients with suspected extremity fractures would have a lot of pain. If you have ever had a painful extremity fracture, you might expect all extremity fractures to be painful. You might also desire that many, most, or even all of these suspected extremity fractures be treated with pain medicine. The authors do not provide anything to support this conclusion.

Let's look at the injuries documented.

All of them seem as if they would be painful fractures. Still, we do not know anything about the pain of these patients.

What else was done that might have acted as pain management?

Supportive medical treatment provided included air splints (25% of patients); full immobilization (19%); ice packs (17%); bandages/dressings (16%); and intravenous lines (9.4%).^[1]

Air splints may help to relieve pain by positioning the extremity in a less painful, assuming there is any pain, position. Splinting may temporarily increase pain during application.

Full immobilization is unlikely to provide any pain relief. Full immobilization on a solid long spine board is expected to increase pain.^[2]

Ice packs can increase pain, decrease pain, or both.

Bandages/dressings might provide some stabilization, or pressure, that decreases the sensation of pain.

Intravenous lines are often painful. If I only suspect an extremity fracture, I would not have any other justification to be starting an IV, except to have a route to deliver IV pain medication. 2 patients received IV pain medication. 94 patients received IV lines. 2/94?

Did one medic start a line, while the other medic contacted medical command. Since The care of each patient is discussed with an online medical control emergency physician in a local emergency department, the superfluous medic may use that time to get online medical control emergency physician contact out of the way, so that the medic can do something useful, such as assessing or treating the patient.

Did the online medical control emergency physician give this counter-order to the medics? Do not follow your standing orders for pain management. Do not give any pain medicine.

Were the medics, or was one of the medics, hesitant to provide any pain medicine without first contacting the online medical control emergency physician?

Are the medics routinely yelled at by emergency physicians if they administer pain medicine without requesting permission first, even though protocols allow them to give pain medicine without asking for permission?

Do administrators receive complaints from emergency physicians when medics follow standing orders for pain medicine?

The number of patients receiving morphine is so small, that I want to know what was so bizarre about these patients that these Just say No! paramedics gave morphine.

Was the morphine given on standing orders?

Was the morphine even given intentionally?

Since giving morphine for suspected extremity fractures is such a freak occurrence in this system, is there any evidence to suggest that these were not 2 medication errors?

Is the occurrence of morphine administration any less rare than the system's occurrence of medication errors?

The use of morphine is so breathtakingly out of the ordinary in this system, that I do not see any reason to conclude that there is any connection between morphine and suspected extremity fracture. Were any other medications, aside from nitrous oxide, given to any of these patients? Were any of those medications given more frequently than morphine? 2/1,000 suspected extremity fractures.

The EMS pain control policy included standing orders for administration of either morphine sulfate (adult dose: 2–5 mg intravenous push [IVP], may repeat x 1; pediatric dose: 0.1 mg/kg) or nitrous oxide (50%), self-administered. The care of each patient is discussed with an online medical control emergency physician in a local emergency department. By protocol, analgesic therapy is contraindicated in patients with the following conditions: altered level of consciousness; alcohol or drug use; allergies to morphine or nitrous oxide; hypotension; head injury; chest injury with suspected pneumothorax; abdominal pain with possible bowel obstruction; symptomatic asthma or chronic obstructive pulmonary disease (COPD); or respiratory distress.^[1]

Even with standing orders, patient care must be discussed with a doctor. In that case, are they really standing orders? There are a lot of contraindications. I almost expect to see suspected extremity fracture listed as a contraindication for morphine. How much different would the results be, if that were the case?

2/1,000 vs 0/1,000.

Is this number, 2/1,000, even close to being statistically significant?

We don't know how many of the 1,000 patients actually had pain that would be appropriate to treat with morphine.

This study examined the use of analgesia in 1,000 prehospital patients with suspected fractures of the extremities who were treated by paramedics. Of the 1,000 patients, only a very few (1.8%) received any pain medication, although morphine sulfate and nitrous oxide were available to the paramedics by both standing order and direct physician order through online medical control.^[1]

I think it is misleading to suggest that there was any encouragement by medical command to treat patients with morphine. However, I have no way of knowing if one, or both, of the patients treated with morphine only received morphine because the doctor ordered it.

My experience with online medical command has been one of repeated refusal to give orders for for pain medicine for patients with pain - pain that I would be authorized to treat on standing orders under my current protocols.

What is the difference?

The patients treated with morphine do not suffer as much. The medical command physician does not get to exercise a medical whim to deny pain medicine purely due to the physician's lack of understanding of pain management.

The mean time spent on the scene for all patients in the study was 23 ±3.4 minutes. Scene times were significantly longer for patients who received pain medication (n = 18) 32.8 ±17.4 minutes, than for those who did not, 22.8 ±10.4 minutes (95% CI 5.22 to 14.58). Transport times to the area hospitals average 7 minutes in this system, with the three main receiving hospitals located in the same geographic area. ^[1]

Unless a patient is unstable (or at risk of injury if not moved), there is no good reason to transport the patient until after the pain is managed. It does not matter if this means an extra 5 minutes on scene or an extra hour on scene. More aggressive dosing (morphine 0.1 mg/kg followed by 0.05 mg/kg every 5 minutes until significant relief) and more appropriate medication (fentanyl at appropriate doses) will result in less time on scene. We should not be manipulating painful injuries until after the pain is managed, unless there is some good reason. That is rare.

When I call for orders for more pain medicine, because the standing orders have not been appropriate in managing pain, medical command often wants to know how far I am from the hospital. My response is, That depends on how quickly I get orders for appropriate pain management, because the patient is not being moved until the pain is managed. Why isn't that obvious to everyone?

Why increase the patient's pain to move the patient to bring the patient to the pain medicine in the hospital, when the patient can be treated just as safely, if not more safely, before being moved?

Second, the administration of nitrous oxide requires that in addition to directly transporting the patient, the paramedics must also exchange the used nitrous tank for a new one. In Akron, the only tank exchange site was located in a remote part of the city, necessitating extended duties and travel time for one of the paramedics. Upon completion of this study, replacement nitrous tanks were placed in each of the 12 fire houses to facilitate more convenient restocking.^[1]

It is good to see that they are trying to make things better for patients by eliminating the excuses used by paramedics, when medics rationalize avoiding treating patients appropriately.

Managing pain in the prehospital setting may require a multifaceted approach. Pain experienced by the patient must be evaluated in an objective manner, and once assessed, managed appropriately. Prehospital care providers should be encouraged to appreciate their patients’ pain and given the tools and affirmation needed to provide the most appropriate care.^[1]

Yes.

CONCLUSION
Prehospital care providers and their medical control supervisors have room to improve the quality of pain control in the prehospital setting. In this review of the use of analgesia for patients with suspected fractures of the extremities, pain medication was rarely used. Improvements in both the recognition and assessment of pain and in treating the pain in the prehospital setting are slow to be implemented. Education, pain control evaluation, protocol development, and quality assurance and audit systems are all measures that can be used to improve the quality of pain management in the prehospital setting.^[1]

All good points, but the most important point is not in there.

Pain management is about treating pain, not treating specific medical conditions.

If you look at all of the contraindications to the use of pain management in this study, there appears to be a strong bias against treating many painful conditions that are not medical contraindications. These appear to be just demonstrations of discomfort with pain management and ignorance of appropriate pain management. As critical as I am of this study, at least the authors are working to improve the way their system manages pain. Most systems seem to deny that there is a problem.

We need to educate prehospital providers to be much more aggressive with pain management.

We spend so much time worrying about paramedics being too aggressive with pain management, but nobody seems to be able to come up with any evidence to support this paranoid fantasy.

We need to provoke medical directors, emergency physicians, emergency nurses, EMTs, and paramedics to take pain seriously.

Footnotes:

^ ¹ Prehospital use of analgesia for suspected extremity fractures.
White LJ, Cooper JD, Chambers RM, Gradisek RE.
Prehosp Emerg Care. 2000 Jul-Sep;4(3):205-8.
PMID: 10895913 [PubMed - indexed for MEDLINE]

^ ² Unnecessary out-of-hospital use of full spinal immobilization.
McHugh TP, Taylor JP.
Acad Emerg Med. 1998 Mar;5(3):278-80. No abstract available.
PMID: 9523943 [PubMed - indexed for MEDLINE]

Standard backboard immobilization is not harmless and can cause significant pain, especially at the occipital prominence and lumbosacral areas. Within 10 minutes of being placed in FSI, Hamilton and Pons¹² showed that volunteers developed moderate to severe pain. After 30 minutes in FSI, Chan et al.¹³ found 100% of volunteers complained of pain, with 55% of the group grading their pain as moderate to severe in quality. Interestingly, 29% of the subjects developed new symptoms over the course of the next 2 days. Chen et al. concluded that “the standard process of immobilization may complicate the evaluation of the trauma patient by generating additional symptoms . . . leading to unnecessary laboratory tests and radiographic studies, time of immobilization, and ultimately, health care costs.” In addition to pain, FSI can cause changes in pulmonary function. can cause pressure ulcers of the buttocks, scalp, or neck, and can increase the risk of aspiration after vomiting.¹³,¹⁴ Because standard FSI can compromise maternal and fetal circulation, it is relatively contraindicated in gravid women.

^ ¹² The efficacy and comfort of full-body vacuum splints for cervical-spine immobilization.
Hamilton RS, Pons PT.
J Emerg Med. 1996 Sep-Oct;14(5):553-9.
PMID: 8933314 [PubMed - indexed for MEDLINE]

^ ¹³ The effect of spinal immobilization on healthy volunteers.
Chan D, Goldberg R, Tascone A, Harmon S, Chan L.
Ann Emerg Med. 1994 Jan;23(1):48-51.
PMID: 8273958 [PubMed - indexed for MEDLINE]

^ ¹⁴ A review of spinal immobilization techniques.
De Lorenzo RA.
J Emerg Med. 1996 Sep-Oct;14(5):603-13. Review.
PMID: 8933323 [PubMed - indexed for MEDLINE]

EMS Week 2010

2010-05-17T21:56:00.002-04:00

Happy EMS Week everyone!!!

In the comments, please provide your most memorable experience from this last year of being an EMSer.

The following video was something provided by (the old) Rocky Mountain Medic. He was a fellow EMS blogger, and wanted this shared for EMS Week.

67 y/o male CC: Syncope

2010-05-17T13:10:00.006-04:00

Also posted over at 12-Lead ECG Blog, go check out all the other great stuff there!

A 67 y/o male has fallen to the ground at his residence. His "partner" called 911 after seeing that he was unconscious. Upon your arrival the patient is alert and requesting that you pick him up because he really needs to make a bowel movement. The patient denies syncope but states that he does not remember falling.

Here is the initial ECG and the subsequent 12-lead ECG. Sorry for the poor quality.

What do you see?

What do you want to know?

What do you want to do?

****Update****

His Vital Signs

HR correlates with monitor, pulse not palpable at radial.

Initial BP 78/60

AAOx3, normal mental status, just wants to make a bowel movement.

Skin - Pale, more pronounced and white from the waste down. Skin was relatively dry.

****Update 5/20/2010****

A new 12-lead ECG is captured during transport.

The patient's vital signs do not improve dramatically with IV fluids.

****Update 5/23/2010****

During transport the patient's condition declined rapidly. After the 12-lead ECG above was captured, the patient went in to a decorticate posture. As most of you know, this is indicative of some sort of neuro compromise. With his airway control, mental status, and respiratory rate all declining, brainstem herniation was at the top of the list of differentials.

The patient became pulseless and apneic just prior to arriving at the ER--according to my partners, just after he released the bowel movement. The patient was not revived.

So what happened here?

Me and the field training officer came up with a few possible solutions. First, there is ST-elevation in the inferolateral leads of the initial 12-lead ECG. With the hypotension, a RCA occlusion is a possibility. If the patient has a dominant RCA, there appears to be some ST-depression in the septal leads, but this is a RBBB pattern, so with the T-wave discordance, the ST-depression is not a good clinical indicator of posterior wall involvement.

First Possibility: Right-sided infarct with hemodynamic compromise leading to a syncopal episode. The syncope caused a secondary head injury which cerebrally herniated during transport. I would like to note that this is highly unlikely. Also, the patient did not improve with fluids, which would have happened with a traditional RV infarct.

Second Possibility: It is much more likely that the patient had an atypical hemorrhagic stroke that presented with the first symptom of syncope. The changes on the 12-lead ECG could just be concurrent with cerebral ischemia. This is not completely understood, but theories involving nerve endings in the myocardium are abundant. The patient's ICP would have increased during transport with the final result being cardiac arrest.

Third Possibility: Abdominal aortic aneurism with severe secondary cerebral ischemia due to hemodynamic instability. I'm not fond of this idea even though the AAA fit the picture in the beginning, it does not explain the decorticate posturing.

We also keep the huge possibility that we have no idea what happened on the list. Ok, so I wish I had more to give you, but an autopsy was not performed on this patient. It remains a mystery.

Improving AHA

2010-05-16T18:02:00.002-04:00

Those of you who follow the Paramedicine 101 Facebook fan page may have noticed a discussion, after this post was shared on the wall. A follower mentioned the AHA Learn: Rapid STEMI ID course, and how it could be a solution. Myself, and Tom B then casually shared some choice opinions about video-based AHA courses. I recently received an email from the commenter, who happens to be affiliated with the AHA. He humbly asked if he could call me regarding my ideas. I suggested a conference call with Tom, and he suggested a conference call with the people whom make decisions at AHA. If we do get them to take interest, I would like to be able to provide a lot of insight. I have many ideas, but would like to solicit some more from our faithful readers.

How do you feel AHA courses could improve?

- ACLS

- CPR

- PALS

- Rapid STEMI ID

Please provide any suggestions. This is our chance to make a difference. RM, don't hold back.

MedicCast - EMS and Health Care Workplace Violence on Federal Radar

2010-05-16T01:05:00.002-04:00

Jamie Davis at the MedicCast writes - EMS and Health Care Workplace Violence on Federal Radar. He also refers to a MedicCast podcast that has not yet been posted, but will be worth listening to when it is posted.

I completely agree with what he writes.

As with people who are not convicted of crimes, because of extenuating circumstance (such as a low blood sugar), the lack of conviction does not mean that the violence did not happen. The lack of a criminal conviction does not mean that nobody was hurt or killed. The lack of a criminal conviction does not even mean that an arrest was inappropriate.

We are covering up violence by not reporting violence.

We are encouraging violence by not reporting violence.

We are pretending that violence that did not result in hospitalization did not happen. Then we are surprised when there is violence that results in hospitalization. When we provide excuses, we encourage excesses.

This is also a problem in the hospital. Nurses are discouraged from reporting violence and from pressing charges. We need to do a much better job of reporting violence.

I continually criticize Zero Tolerance Laws, because the idea that everything in the same category should be treated with at least some punishment completely ignores that the category will include things that do not deserve punishment. On the other hand, I support Zero Tolerance reporting of violence.

Translated from French, the painting states, This is not a pipe. This is true, since it is a picture of a pipe. Rene Magritte's The Treachery Of Images is often used to make this point.

If a picture of something were the same as the object portrayed, I would take this picture of gold bars from Fort Knox to someone who could pay me for the gold. This would quickly destabilize civilization, which would not be a good thing. As it turns out, the image is from an article about fake gold bars in Fort Knox. How would we be able to tell the difference between a picture of the real thing and a picture of a fake? Since a fake is creating an image of the real thing, would it matter?

How is this relevant?

One of the problems with Zero Tolerance Laws is that they do not make this distinction between reality and appearance.

Zero Tolerance Laws mandate punishment for a politically incorrect appearance.

Zero Tolerance Laws discourage judgment - Sentence first, verdict afterward.

Zero Tolerance Laws are designed to prevent us from thinking, because What if somebody makes a bad decision?

Zero Tolerance Laws are excellent examples of extremely bad decisions.

Zero Tolerance reporting helps to make us aware of the problem and helps to do something about the problem.

Zero Tolerance reporting of violence is a way to learn just how bad a problem is.

Zero Tolerance reporting of violence is a way to prevent violence from being ignored.

Assaults on medical personnel are a real problem.

Assaults on medical personnel are not imaginary.

We need to start acting as if the lack of reporting of violence means that violence is not real.

Today, Magritte might paint a picture of an assault on a doctor/nurse/EMT and write This is not a reported assault. Imagine if we were to do something completely crazy - imagine if we were to face reality.

Go read what Jamie wrote. He is the one providing the details about workplace violence and medical personnel.

.

26 year old male CC: Chest pain

2010-05-14T06:56:00.001-04:00

Here's a great case submitted by a faithful reader who wishes to remain anonymous.

EMS is called to a 26 year old male complaining of chest pain.

On arrival patient is found sitting on his living room couch. He appears anxious and acutely ill.

He states that he was riding his bike when he became anxious, had a "coughing spell" and started to experience chest discomfort. The location of the chest discomfort is in the center of his chest and slightly to the left.

Onset: Sudden while riding a bike

Provoke: Nothing makes the pain better or worse

Quality: Difficult to describe but with prompting the patient calls it "pressure"

Radiate: Left jaw and left arm

Severity: 7/10

Time: No previous episodes

The patients skin is warm and moist. The color is normal.

The patient denies shortness of breath. Breath sounds are clear bilaterally.

He is nauseated but he has not vomited.

Past medical history: Healthy

Medications: None

Vital signs are assessed.

Resp: 22

Pulse: 98

BP: 140/84

SpO2: 100 with oxygen via NRB @ 15 LPM

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your impression?

*** Update 05/14/2010 ***

The importance of serial ECGs cannot be over-emphasized.

In this case, a second 12-lead ECG was captured just prior to arrival at the hospital.

Does this new information shed any light on the probably diagnosis?

What else could you have done?

Prehospital 12-Lead ECG Efficiency

2010-05-12T22:38:00.005-04:00

Recently I have taken part in a very interesting discussion on the NAEMSP dialog page. This discussion is based on the paper Early Cardiac Cath Lab Activation by Paramedics for Patients with STEMI on Prehospital 12 Lead ECGs. Tom B from The Prehospital 12-Lead blog, and contributing author to Paramedicine 101 is one of the active participants in the discussion.

Some of the problems discussed:

- Poor quality ECG captures

- Deficiency in knowing when to capture a 12-lead ECG (43% of paramedics in one study did not perform a 12-lead on an active STEMI)

- Deficiency with STEMI recognition (False positives are still far to frequent)

- Poor STEMI alert and transport guidelines

One of the solutions which has a lot of supporting evidence is the transmission of 12-lead ECGs from the field to the receiving PCI facility.

Some research:

THE POSITIVE PREDICTIVE VALUE OF PARAMEDIC VERSUS EMERGENCY PHYSICIAN INTERPRETATION OF THE PREHOSPITAL 12-LEAD ELECTROCARDIOGRAM

Background. Obtaining a prehospital 12-lead ECG may improve triage and expedite care of patients with acute myocardial infarction (AMI). Whether the ECG should undergo physician review prior to activation of a percutaneous intervention (PCI) team is unclear. Objective. To document the positive predictive value (PPV) of the prehospital 12- lead ECG when interpreted by paramedics versus emergency physicians. Methods. This was a prospective, observational study. In November 2003, our local health care and emergency medical services (EMS) systems implemented a prehospital “cardiac alert” program in which patients suspected of having ST-elevation myocardial infarction (STEMI) based on the prehospital 12-lead ECG were diverted away from receiving facilities without emergent PCI capability and the PCI team was mobilized. For the first year, a cardiac alert was activated by paramedics (Phase I). After the first year, the ECG was transmitted to the ED, with the emergency physician (EP) responsible for activation (Phase II). The PPV for cardiac alerts in Phases I and II were compared by using three different “gold standards”: cardiologist interpretation of the prehospital 12-lead ECG, disposition to emergent PCI, and coronary lesions on angiography or arrest prior to emergent PCI. Results. A total of 110 patients were enrolled (54 in Phase I, 56 in Phase II). Cardiologist confirmation of a STEMI on the prehospital 12-leadEKGwas 42/54 (78%) in Phase I and 54/56 (96%) in Phase II. Disposition to emergent PCI occurred in 38/54 (70%) Phase I patients and 51/56 (91%) Phase II patients. Lesions at catheterization or arrest prior to emergent PCI were observed in 41/54 (69%) of Phase I patients and 50/56 (89%) of Phase II patients. All of these comparisons achieved statistical significance (p less than 0.01) Conclusions. Transmission to the ED for EP interpretation improves the PPV of the prehospital 12-lead ECG for triage and therapeutic decision-making.

-PREHOSPITAL EMERGENCY CARE 2007;11:399–402

Okay so a solution I would like to provide, and please provide comments here and/or on the dialog page linked to above.

My solution is to provide an adjunct course. Much like ACLS, CPR, PALS or BTLS, this course could be taught in conjunction with the paramedic curriculum but will expire and renewals would be required. The current paramedic curriculum does not include enough instruction on prehospital 12-lead ECG interpretation. My proposed course would include a whole lot more information as well as STE-Mimic recognition. Why not? In my experience, I have noticed that the biggest deficiencies that paramedics present are airway, medication administration, and cardiac rhythm interpretation--especially 12-lead ECG interpretation.

So what do you think?

Provide your thoughts or your solutions to narrowing the EMS to repurfusion times.