Pharmacology | Rogue Medic

If you have a BVM (Bag Valve Mask resuscitator), you should not need naloxone. The problem is inadequate respiration, not inadequate naloxonation.

- Rogue Medic

Drug Shortage Update Affecting a Lot of the Ex-Code Drugs

Wed, 16 May 2012 11:00:57 +0000 By Rogue Medic Leave a Comment

Today’s drug shortage update from the FDA (Food and Drug Administration) includes a lot of drugs that used to be routine drugs for cardiac arrest.

Once upon a time, I was a code drug.

Atropine is the most recent drug to be dumped by the AHA (American Heart Association). In the past week, two manufacturers have stated that they have atropine available. FDA Update.

It was nice to see the AHA admit that there is not a good reason to keep treating every PEA (Pulseless Electrical Activity) or asystole patient with a drug that has never had good evidence that it improves survival. The next revision of the ACLS (Advanced Cardiac Life Support) guidelines will provide more opportunity to get rid of some drugs that are routinely used for cardiac arrest, even though there is no evidence that they improve survival – lidocaine (farther down on this list), amiodarone, and the everybody’s favorite drug to not improve survival – epinephrine (also farther down on the list).

Calcium Chloride has increased availability from one manufacturer, but decreased availability from another. Calcium is still the best drug for hyperkalemia, but it was once used routinely in cardiac arrest, as if there has been a lot of sudden onset hypocalcemia. FDA Update.

Epinephrine 1:10,000 has not yet been dumped by the FDA, but the recent evidence suggests that we are decreasing survival by using epinephrine – and those who do survive the epinephrine are more likely to have significant brain damage. FDA Update

Tomorrow, I will be talking about the evidence for and against epinephrine at the EMS Web Summit.

Lidocaine has new manufacturing delays. Lidocaine is still just barely in the ACLS guidelines –

Amiodarone may be considered when VF/VT is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE A). If amiodarone is unavailable, lidocaine may be considered, but in clinical studies lidocaine has not been demonstrated to improve rates of ROSC and hospital admission compared with amiodarone (Class IIb, LOE B).^[1]

Maybe lidocaine is there to make amiodarone look good, because nothing else makes amiodarone look good.

For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge.^128,–,133 In comparison, other ACLS therapies such as some medications and advanced airways, although associated with an increased rate of ROSC, have not been shown to increase the rate of survival to hospital discharge.^{31,33,134,–,138} ^[2]

In other words, these drugs are probably only as effective as atropine, and maybe less harmful than atropine, but the AHA has not given up on them, yet. FDA Update.

Magnesium Sulfate is another once-promising code drug, now used for the ever-impressive torsades and for the less impressive hypomagnesemia. FDA Update

Sodium Bicarbonate used to be given almost as much as epinephrine.

Now, Sodium Bicarbonate is only given when it is specifically indicated – the way that real medicine should be used.

Sodium Bicarbonate is second line for hyperkalemia and probably is just the hypertonic saline (5.8% saline) that is working, rather than treatment of acidosis, but acidotic patients may benefit from that, too – if they are well ventilated. Sodium Bicarbonate is CO₂ in a syringe.

FDA Update.

Vasopressin is now available, again. Not useful in cardiac arrest, but we feel we need to inject something, so this permits some variety. FDA Update.

Important non-code EMS drugs on the FDA Current Drug Shortages list are:

Alfentanyl – Possibly substituting for fentanyl, but not having enough to make up for the lack of fentanyl. Probably also due to increased realization that the side effects of opioids are easily managed by competent medical personnel.

Atracurium (Tracrium).

Diazepam (Valium).

Digoxin.

Diltiazem (Cardizem).

Diphenhydramine (Benadryl).

Etomidate (Amidate).

Fentanyl (Sublimaze).

Hydromorphone (Dilaudid).

Ketorolac (Toradol).

Lorazepam (Ativan).

Mannitol.

Metoclopramide (Reglan).

Midazolam (Versed).

Morphine.

Multi-vitamin injection (banana bags?).

Naloxone (Narcan).

Naltrexone.

Ondansetron (Zofran).

Oxytocin (Pitocin).

Pancuronium (Pavulon).

Phentolamine (Regitine).

Procainamide (Pronestyl) – the only ventricular antiarrhythmic that works (of those commonly available in the US – [sotalol also works]).

Prochlorperazine (Compazine).

Promethazine (Phenergan)

Propofol (Diprivan).

Sufentanyl (Sufenta).

Tromethamine (Tham).

Vecuronium (Norcuron).

and something new –

Sodium Chloride 0.9% (5.8mL and 20mL) (Initial Posting Date) – 5/4/2012. FDA Update.

Footnotes:

^[1] Drug Therapy in VF/Pulseless VT
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Advanced Life Support
Part 8.2: Management of Cardiac Arrest
Free Full Text from Circulation

^[2] Overview
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Advanced Life Support
Part 8.2: Management of Cardiac Arrest
Free Full Text from Circulation

Filed Under: 2010 AHA Guidelines, FDA, Heresy, Pharmacology

Influence of Sex on the Out-of-hospital Management of Chest Pain – Part II

Tue, 15 May 2012 08:00:22 +0000 By Rogue Medic Leave a Comment

Part I was written in 2010, so I am a bit late in continuing to ridicule this example of bad research.

How do we determine what is good care for our patients?

By having our treatment follow the category that dispatch dispatch assigned the call? I used to work in a county, where this did appear to be the case. The medics would become very upset with dispatch if they did not receive a lot of information about the patient prior to arriving on scene.

Dispatchers would express surprise when I would tell them that I did not care about the information they could obtain over the telephone from some unknown person.

Why?

Apparently, these medics never learned to assess patients themselves.

We conducted a population-based retrospective cohort study of 800 randomly selected patients over the age of 30 years for whom EMS were dispatched for a complaint of chest pain during a single year.^[1]

These are not patients with a medical complaint of chest pain, but patients dispatched as chest pain – for whatever reason.

These are not patients considered to be cardiac by the emergency physician, but patients dispatched as chest pain.

The main outcome was adherence to state EMS protocols for treatment of patients over age 30 years with undifferentiated chest pain. Rates of administration of aspirin, nitroglycerin, and oxygen; establishment of intravenous (IV) access; and cardiac monitoring were measured.^[1]

Should we give aspirin (as a cardiac treatment) to patients who do not have, and never did have, chest pain?

Should we give nitroglycerin (as a cardiac treatment) to patients who do not have, and never did have, chest pain?

The role of dispatch is not to determine the treatment for the paramedics or for the physicians. The role of dispatch is to prioritize getting the right people to the patient in the right amount of time.

What information do I want from dispatch?

How many patients they believe are there.

Trauma vs medical.

Reports of any violence or anything suspicious of violence.

Who else is responding.

Any reports of traffic problems in the area, or other unusual events that might affect what we do.

Unusual (or amusing) things picked up during the phone call.

The location of the patient.

Should there be any more of an exchange of information than the following?

Respond to location X for an adult with chest pain. X is also responding.

10-4.

Dispatch has more important things to do than to do assessments for incompetent medics.

According to the authors of the study, if dispatch mentions chest pain, I am supposed to follow my Suspected ACS (Acute Coronary Syndrome) protocol, even though that protocol does not mention anything about receiving medical direction from dispatch. The protocol begins with the words, Initial patient contact. Why doesn’t the protocol begin with Dispatch Diagnosis?

I work in the same state. The protocols have changed since the study, but dispatch is only mentioned three times in my paramedic protocols. All of these times are only related to cardiac arrest.

Maybe I will write a Part III. Maybe, if I do write it, it will not take over two years.

Footnotes:

^[1] Influence of sex on the out-of-hospital management of chest pain.
Meisel ZF, Armstrong K, Mechem CC, Shofer FS, Peacock N, Facenda K, Pollack CV.
Acad Emerg Med. 2010 Jan;17(1):80-7.
PMID: 20078440 [PubMed - indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine

Meisel, Z., Armstrong, K., Crawford Mechem, C., Shofer, F., Peacock, N., Facenda, K., & Pollack, C. (2010). Influence of Sex on the Out-of-hospital Management of Chest Pain Academic Emergency Medicine, 17 (1), 80-87 DOI: 10.1111/j.1553-2712.2009.00618.x

Filed Under: ACS, Cardiology, Heresy, Irrational Government Oversight, Pharmacology, Research Blogging

Doesn’t that study prove Lasix works?

Thu, 10 May 2012 15:00:13 +0000 By Rogue Medic 3 Comments

P responsed to Blood volume prior to and following treatment of acute cardiogenic pulmonary edema with the following –

Could you elaborate a little bit on why you included this study? Was it just to point out that Lasix does not work the way many in EMS think it does?

There are two reasons I chose this study.^[1] It provides evidence that the reason for giving furosemide (Lasix – frusemide in Commonwealth countries) to the unstable CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) patient is not valid.

The other reason is the age of the article. We have a long history of ignoring the evidence that the problem is not too much fluid in the patients, but a problem of the fluid being in the wrong places.

Or rather, that in EMS we are taught an incorrect mechanism for Lasix.

I did not really address the possible mechanisms by which furosemide might work, but I will in looking at other research.

Chronic CHF and acute CHF are not the same condition, even though they share many features.

I don’t think furosemide works for patients with acute CHF.

I think furosemide makes things worse for patients with acute CHF.

I will write more about this using other articles, many of which have been around for decades, but have been ignored because too many of us just know it works.

I understand why Lasix has largely fallen out of favor for the treatment of acute CHF, but reading through the actual study it seems like this supports the use of Lasix.

You ask an excellent question.

The study does give the impression that furosemide improved outcomes, but it was never designed as a study of whether furosemide is helpful, or even just not harmful. Other than oxygen, morphine, and furosemide (apparently in that order) we do not know much about the treatment of this small group of patients. Even pulmonary suction is listed as a treatment, but there are no suggestions that treatments are even limited to those listed. (PE = Pulmonary Edema in this case, not Pulmonary Embolism)

Studies were performed in 21 patients, 11 men and 10 women, ranging from 44 to 83 (median 67) years in age. In 16 of the patients, PE was observed at the time of admission to the Center for the Critically Ill and in five patients, PE appeared during the course of in-patient care.^[2]

Previous history of acute pulmonary edema was elicited in nine of the 21 patients; 11 patients had been treated with diuretics prior to the occurrence of acute pulmonary edema; and six patients had evidence of peripheral edema on admission.^[2]

The initial set of measurements were obtained immediately after referral to the Center for the Critically Ill from either the emergency department or general medical services following onset of acute PE. Oxygen was the only agent administered prior to the initial set of measurements.^[2]

This is something I did not pay attention to when writing the first post. These appear to be ICU (Intensive Care Unit) patients. I had mistakenly assumed these were ED (Emergency Department) patients. This also weakens the conclusions I was drawing from the study. I had been reading the Center for the Critically Ill as a fancy name for the ED.

11/21 patients. These patients had a very high rate of the pink, frothy sputum we were told to expect from CHF.

In 11 patients, there was expectoration of frothy fluid.^[2]

Whatever treatment was given to the patients in the ED does not appear to have helped, but we have no idea what the denominator is.

Treatment included oxygen administered by rebreathing mask, ventimask, or nasal prongs in oxygen concentrations ranging from 28 to 60 (mean 40) %. After an initial set of measurements had been obtained, morphine sulfate was injected intravenously in bolus doses ranging from 2 to 5 mg with total dose ranging from 5 to 15 mg until acute anxiety was relieved.^[2]

This is prior to any furosemide (maybe not the total doses of morphine, but the initial doses). If we wanted to see the effects of furosemide, there would be some control of any differences in treatment. There would be more documentation of differences.

Bilateral moist rales and radiographic signs of grade 3 or 4 pulmonary edema, according to the criteria of Turner, Lau, and Jacobson,¹⁰ were documented in each instance.^[2]

This suggests that there is good objective evidence that these patients really did have CHF, which is an important point.

Furosemide was administered by intravenous bolus injection in amounts of 40 or 80 mg. Additional doses of 40 or 80 mg of furosemide were administered after 1 hour in the absence of a diuretic response. The total dose of furosemide during the initial 24 hours of management ranged from 40-160 (mean 71.4) mg.^[2]

How many patients did not have a diuretic response (make urine) in the first hour after receiving furosemide?

We do not know, and the mean of 71.4 mg, with an initial dose of 40 or 80 mg and 40 or 80 mg increments, leaves a lot of room for speculation.

Is that what happened? Did half of the patients receive repeat doses?^[3]

As I stated, I am only speculating, but I could come up with a variety of dose combinations that would produce a similar total mean dose. The point is that this information is not helpful for evaluating the possible effect of furosemide.

Why would patients not have a diuretic response for over an hour after furosemide?

Isn’t furosemide supposed to act like Kryptonite (is there yellow Kryptonite?^[4]) to the fluid retention of CHF?

Aren’t we supposed to keep urinals and bedpans ready for these patients?

If the patient is shunting blood away from the less critical organs, during times of critical illness, how is the furosemide supposed to get to the kidneys quickly?

In patients with chronic heart failure and especially in the presence of generalized edema, prior investigations have demonstrated either increases in intravascular volume^17-19 or no consistent changes.²⁰ During acute cardiogenic pulmonary edema, however, blood volume is more frequently reduced.^[2]

If the patient is stable, drawing off this excess water seems to help to prevent fluid from leaking into the lungs. Should we assume that furosemide preferentially removes fluid from the lungs in patients who are already intravascularly volume depleted?

Accordingly, plasma water had been removed from the intravascular compartment. The evidence points to extravasation of fluid from the intravascular compartment that is low in colloid content. The likelihood that this represents, at least in part, fluid which is extravasated into the lung is consistent with observations on the protein content and colloid osmotic pressure of pulmonary edema fluid.^[2]

If the solution were removal of the patients’ already low intravascular volume and furosemide could be shown to have a rapid diuretic effect, furosemide would probably be useful.

Can these patients really wait more than an hour to breathe?

If furosemide could be shown to produce some sort of vasodilation, furosemide would probably be useful, even if the diuresis were not the method.

At another time, I will write about the way furosemide causes vasoconstriction – which is the opposite of the effect we are told furosemide produces.

For evaluating the efficacy of furosemide, this study has too many unknowns. The authors never intended to study the efficacy of furosemide, so that is not a problem of poor study design. Their study was designed to find out something else.

Footnotes:

^[1] Blood volume prior to and following treatment of acute cardiogenic pulmonary edema.
Figueras J, Weil MH.
Circulation. 1978 Feb;57(2):349-55.
PMID: 618625 [PubMed - indexed for MEDLINE]

Free Full Text Download from Circulation in PDF format

^[2] Blood volume prior to and following treatment of acute cardiogenic pulmonary edema.

The same study as above.

^[3] Speculation on possible dosage combinations –

We do not know, and the mean of 71.4 mg, with an initial dose of 40 or 80 mg and 40 or 80 mg increments, leaves a lot of room for speculation.

I am putting some speculation down here, since it does take up a lot of room and may not be of interest to many people.

We do not know how many had an initial dose of 40 mg. If 20 of the patients received 40 mg and one patient received 80 mg, then the mean initial dose would be 41.9 mg.

If 20 of the patients received 40 mg and one patient received 80 mg, and every patient received one repeat of their initial dose (20 x 40 mg and 1 x 80 mg), then the mean total dose would be 83.8 mg. Most of the patients could have received repeat doses after an hour of no diuresis.

On the other hand, if one patient received 40 mg and 20 of the patients received 80 mg, then the mean initial dose would be 78.1 mg. Each initial 40 mg dose would make the total mean dose almost 2 mg higher.

What if 5/21 received 80 mg initially and no further doses; 11/21 received 40 mg and each received a second 40 mg dose; and 5/21 received only a 40 mg initial dose?

This would produce a total mean dose of 70.5 mg, which is close to the actual total mean dose of 71.4 mg.

Is that what happened? Did half of the patients receive repeat doses? As I stated, I am only speculating, but I could come up with a variety of dose combinations that would produce a similar total mean dose. The point is that this information is not helpful for evaluating the possible effect of the medication.

^[4] Kryptonite
Wikipedia
Variations
Article

More than I ever wanted to know about Kryptonite. There is a gold Kryptonite. There is even a yellow hoax Kryptonite. Could either of these be made of furosemide?

Figueras J, & Weil MH (1978). Blood volume prior to and following treatment of acute cardiogenic pulmonary edema. Circulation, 57 (2), 349-55 PMID: 618625

Filed Under: Heresy, Pharmacology, Research Blogging

Should We Lie To Patients?

Wed, 09 May 2012 15:20:24 +0000 By Rogue Medic 3 Comments

This on EMS Office Hours, Jim Hoffman, Josh Knapp, and I discuss whether it is ever appropriate to lie to patients.

Should We Lie To Patients?

Why do we assume that we know what the truth is?

I KNOW that you are having a heart attack!

Maybe.

Do any of us have 100% accuracy at identifying STEMIs (ST segment Elevation Myocardial Infarctions)?

What about NSTEMIs (Non-ST segment Elevation Myocardial Infarctions)? They are still heart attacks, but they don’t go straight to the cardiac catheterization lab. Just because we don’t take them to the same place, does that mean that it isn’t a heart attack?

Are cardiologists perfect at identifying heart attacks?

So, how can we claim that we KNOW that someone is having a heart attack. We understand that the probability is very high, but that is not certainty.

Why do we assume that we need to present an impression of certainty?

Certainty = Self-Delusion.

For example, the topic of the necessity of giving oxygen to patients presenting with ACS (Acute Coronary Syndromes – possible heart attacks).

Crushing sub-sternal chest pain radiating to the arm and jaw, 10/10 pressure. No cyanosis. No shortness of breath. SpO₂ = 96%.

Is oxygen indicated?

EMS providers administer oxygen during the initial assessment of patients with suspected ACS. However, there is insufficient evidence to support its routine use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to ≥94% (Class I, LOE C).³⁶ ^[1]

The horror! The horror!

No EMS protocols would ever suggest that!

Image credit.

From my protocols –

Post resuscitation care

Administer oxygen (titrate to minimum O₂ needed to achieve SpO₂ >94%)^[2]

Yellow highlights are changes in the protocol, even if only changed to clarify something.

What about difficulty breathing?

Administer oxygen at high-flow rate to all patients in severe respiratory distress. COPD patients NOT in respiratory distress should be given oxygen to maintain adequate O₂ saturation (e.g. >90%).^[3]

But you haven’t answered the question about oxygen for chest pain.

3. Administer oxygen by appropriate method and monitor Pulse Oximetry. Place patient in position of comfort. Nasal cannula may be utilized if patient is unable to tolerate a facemask.^[4]

The question of what to tell a psych patient also came up.

Because we know they are going to psych.

Therefore it would be wrong to lie to the patient and suggest that we are not certain that they are going to psych.

Well, . . .

Unless the patient’s behavior is due to something that is not psychiatric –

The literature shows that up to 63% of patients with symptoms classically associated with psychiatric illness have primary or co-morbid medical disease (7–10). One study found that 24% of patients admitted to a neuro-psychiatric unit had their initial diagnosis later changed from a psychiatric to a medical one, or vice versa (11). Some authors suggest that between 44% and 83% of patients erroneously admitted to a psychiatric facility could have been better identiﬁed and redirected by an appropriate physical assessment (4,12). Eight percent of the misdiagnoses had unaddressed abnormal VS (12).^[5]

I do not know that the patient is going to psych.

It would be a lie to pretend that I know what will happen in the hospital.

Go listen to the podcast.

Footnotes:

^[1] Part 10: Acute Coronary Syndromes
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Prehospital Management
Initial EMS Care
Free Full Text from Circulation

^[2] Post-Resuscitation Care
Pennsylvania Statewide Advanced Life Support Protocols
3080 – ALS – Adult/Peds
Pages 34-36/128
Free Full Text PDF of All ALS Protocols

^[3] Asthma/COPD/Bronchospasm
Pennsylvania Statewide Advanced Life Support Protocols
4022 – ALS – Adult/Peds
Pages 48-49/128
Free Full Text PDF of All ALS Protocols

^[4] Suspected Acute Coronary Syndrome
Pennsylvania Statewide Advanced Life Support Protocols
5001 – ALS – Adult/Peds
Pages 52-53/128
Free Full Text PDF of All ALS Protocols

^[5] “Medically cleared”: how well are patients with psychiatric presentations examined by emergency physicians?
Szpakowicz M, Herd A.
J Emerg Med. 2008 Nov;35(4):369-72. Epub 2008 Jul 23.
PMID: 18650052 [PubMed - indexed for MEDLINE]

Filed Under: Assessment, Cardiology, Critical Judgment, EMS Office Hours, Heresy, Pharmacology

Blood volume prior to and following treatment of acute cardiogenic pulmonary edema

Tue, 08 May 2012 20:15:02 +0000 By Rogue Medic 7 Comments

One of the myths of treatment for CHF/ADHF (Congestive Heart Failure/Acute Decompensated Heart Failure) is that the patients are fluid overloaded. We MUST make the patient pee.

If you want to live, you have to pee!

Image credit.

Pee or die!

This has been studied. all the way back in 1978 –

The normal patients had 22% more total plasma volume.

The normal patients had 21% more total blood volume.

The need to remove fluids is based on what?

It is interesting that this study was of patients treated with oxygen, morphine, and furosemide. Only oxygen is still important in the acute treatment of CHF/ADHF.

There were no significant differences in the parameters measured or calculated between nine patients with prior history of acute pulmonary edema and the 12 patients in whom pulmonary edema occurred for the first time. There were also no significant differences in these parameters between the 11 patients who had been previously treated with diuretics and the remaining ten patients.^[1]

We give have been trained to give furosemide (Lasix – frusemide in Commonwealth countries) because CHF = Too much fluid.

How long do we need to hold on to our myths?

How long can we perpetuate dangerous traditions?

Afterward, these patients need to receive fluid, because we have made them even more dehydrated – for no benefit.

Footnotes:

^[1] Blood volume prior to and following treatment of acute cardiogenic pulmonary edema.
Figueras J, Weil MH.
Circulation. 1978 Feb;57(2):349-55.
PMID: 618625 [PubMed - indexed for MEDLINE]

Free Full Text Download from Circulation in PDF format

Figueras J, & Weil MH (1978). Blood volume prior to and following treatment of acute cardiogenic pulmonary edema. Circulation, 57 (2), 349-55 PMID: 618625

Filed Under: Cardiology, Heresy, Mythology, Pharmacology, Research Blogging

The Benefits of Lasix in CHF

Mon, 07 May 2012 20:00:10 +0000 By Rogue Medic Leave a Comment

Furosemide (Lasix) does not improve outcomes for the very sick CHF (Congestive Heart Failure or ADHF – Acute Decompensated Heart Failure) patients.

There are basically three mechanisms for CHF –

PRE-load
Contractility
AFTER-load

The problem is not the PEE-load, unless there is some anatomic connection between the kidneys and the lungs that I do not know about

But what about the circulatory system? The circulatory system connects the lungs and the kidneys and allows the kidneys to remove fluid from the circulation, which allows the fluid to wander out of the lungs.

No.

Stable patients seem to tolerate Lasix well, but these patients will tolerate almost anything we do to them.

Unstable patients are a little harder to keep alive.

What happens to the circulation to the kidneys under stress – the kind of stress that one might experience when not able to get enough oxygen?

The kidneys shut down.

Closed for business.

Take your Lasix somewhere else.

Comeback after the patient’s kidney circulation is open for Lasix again.

Image source.
.

Filed Under: Cardiology, Heresy, Lasix, Pharmacology

Safety of prehospital intravenous fentanyl for adult trauma patients

Thu, 03 May 2012 19:00:35 +0000 By Rogue Medic 1 Comment

What prevents us from treating pain appropriately?

Actual adverse effects of pain medicine or unwarranted anxiety, due to exaggerated fears of potential adverse effects of pain medicine?

In 1999, the Emergency Medical Services Outcomes Project identiﬁed prehospital pain relief as a priority outcome and noted that it is one of the most high-impact prehospital interventions that can be performed on the majority of patients.³ ^[1]

Pain management is important. Unfortunately, EMS and emergency medicine have been better at coming up with excuses for not treating pain, than we have been at coming up with good protocols that encourage treating pain.

Our hypothesis was that a single dose of intravenous fentanyl administered in the prehospital setting would have no detrimental effect on the shock index of initially normotensive adult trauma patients.^[1]

If we appropriately assess our patients, give reasonable doses of fentanyl (or any other pain medicine), is there any good reason to expect that there will be any harm to patients?

If we cannot appropriately assess our patients, what kind of incompetence justifies authorizing us to work as paramedics?

The protocol change allowed paramedics to administer a single 100 µg dose of fentanyl to adult trauma patients being transported “Code 10” (e.g., lights and sirens) to the hospital without a call to the medical command center. No other opioid was allowed for pain management in this population. Before the protocol change, medical command approval was required before administration of fentanyl.^[1]

I see this as even more evidence that medical command permission requirements have nothing to do with protecting patients.

When medical command permission was required, pain management was rare.

After the protocol change patients were almost 6 times more likely to receive fentanyl.

The harm of medical command permission requirements is not controlled for, nor is it a hypothesis of the study. If this does reflect the way that medical command permission requirements discourage, or prevent, appropriate patient care, that raises a question –

How can we justify continuing to allow our patients to be harmed by medical command permission requirements?

Image credit.

Inclusion criteria were (1) age ≥ 18 years; (2) systolic blood pressure (SBP) >90 mm Hg; (3) Glasgow Coma Scale (GCS) score ≥13; and (4) emergent trauma transport to Denver Health Medical Center. Emergent trauma was deﬁned as any “Code 10″ (e.g., lights and sirens) transport to the hospital. Exclusion criteria were pregnancy and imprisonment.^[1]

Pain is not listed as an inclusion criterion.

Severe pain? Moderate pain and severe pain? Abdominal pain? What is permitted on standing orders?

The outcome was the initial ED shock index (deﬁned as the heart rate divided by SBP). As pain relief from fentanyl would typically result in a decrease in both heart rate and blood pressure, the shock index was chosen as a composite outcome for its ability to reﬂect, as a single dependent variable in a multivariable model, abnormal changes in heart
rate and blood pressure.^[1]

This may be a better way to assess vital sign changes than just looking at blood pressure, but is this part of what is used during anesthesia or procedural sedation to assess vital signs?

What if the patient is hypotensive before fentanyl, then receives fentanyl? What if some pain relief produces the expected decrease in heart rate, but the same pain relief also produces an increase in blood pressure?

This study’s protocol would not permit giving fentanyl to hypotensive patients, but that study has already been done –

Click on images to make them larger.^[2] ^[3]

In 47% of cases of administration of fentanyl to already hypotensive trauma patients, the hypotension went away after fentanyl.

Why aren’t we doing larger studies of giving fentanyl to hypotensive patients?

Why are we withholding fentanyl from hypotensive patients?

What if . . . ?

What if we behave intelligently and actually find out?

Perpetuating myths and traditions is bad for patients.

We need to stop the defenders of tradition and mythology from harming our patients.

There is a 97% chance that, after administration of fentanyl to a critical trauma patient who is not hypotensive, the patient will still be not hypotensive.

There is a 47% chance that, after administration of fentanyl to a critical trauma patient who is hypotensive, the patient will be not hypotensive.

If we did not have so much anxiety about fentanyl, we might consider making it the standard of care for hypotension following trauma.

A total of 1,669 patients met criteria for inclusion during the study period.^[1]

This is one of the problems with not fully describing the criteria. Did all of these patients have pain that met the criteria for administration of fentanyl? If so, then giving fentanyl to only 217 patients (13% of 1,699) is horrible.

Seven patients had an initial ED SBP <90 mm Hg, and all were included in the control group.^[1]

Would fentanyl have prevented those cases of hypotension?

Footnotes:

^[1] Safety of prehospital intravenous fentanyl for adult trauma patients.
Soriya GC, McVaney KE, Liao MM, Haukoos JS, Byyny RL, Gravitz C, Colwell CB.
J Trauma Acute Care Surg. 2012 Mar;72(3):755-759.
PMID: 22491566 [PubMed - as supplied by publisher]

^[2] Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia.
Krauss WC, Shah S, Shah S, Thomas SH.
J Emerg Med. 2011 Feb;40(2):182-7. Epub 2009 Mar 27.
PMID: 19327928 [PubMed - in process]

Full Text PDF Download at medicalscg.

Fentanyl Study: EMS Research Episode 9
EMS Research Podcast
Podcast page

^[3] Chart Version – Fentanyl in the out-of-hospital setting: variables associated with hypotension and hypoxemia
Sun, 05 Jun 2011
Rogue Medic
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Soriya GC, McVaney KE, Liao MM, Haukoos JS, Byyny RL, Gravitz C, & Colwell CB (2012). Safety of prehospital intravenous fentanyl for adult trauma patients. The journal of trauma and acute care surgery, 72 (3), 755-759 PMID: 22491566

Filed Under: Fentanyl, Heresy, OLMC Requirements, Pharmacology, Research Blogging

Lessons for management of anaphylaxis from a study of fatal reactions – Part I

Thu, 26 Apr 2012 10:00:39 +0000 By Rogue Medic 13 Comments

Also posted over at Research Blogging.

What can help us to learn more about what leads up to a bad outcome from anaphylaxis?

it seemed that study of a large number of fatal reactions might give insight into why prevention and treatment had failed.^[1]

Most of these patients are old. The young seem to be clustered in exposures to nuts and other food allergens.

Click on images to make them larger.

Only nine of these patients did have epinephrine anaphylaxis kits prescribed. Most were not used. The use/lack of use is documented in this table –

For most of the anaphylaxis that was not due to food, the cause of death was considered to be shock, or a combination of respiratory compromise and shock. For the anaphylaxis related to food, the opposite was true. None were considered to be just due to shock and only 5 out of 37 were considered to be due to a combination of respiratory compromise and shock.

Is this representative of the deaths from anaphylaxis?

It is not clear what fraction of the total number of fatal reactions have been identified; unidentified cases will include those dying from acute asthma due to unrecognized food allergy [13], sudden death from unrecognized insect stings [14] and elderly bronchitics dying at home from unrecognized antibiotic anaphylaxis [15]. ^[1]

A major problem is the lack of recognition of anaphylaxis, even by paramedics.

The first treatment for noniatrogenic reactions was in some cases given by paramedics. Because all food-related reactions caused dif®culty breathing, the paramedics commonly had difficulty deciding whether to use the protocol for anaphylaxis or for asthma. This led to delayed or inappropriate treatment that may have contributed to the fatality. Paramedic protocols should allow for this difficulty [18]. ^[1]

For those of us who still might think that all we have to do is follow the protocol, some of these patients were treated by paramedics who followed protocol. Unfortunately, they did not follow the anaphylaxis protocol.

One physician assumed that the patient was just hyperventilating withheld epinephrine (adrenaline) because the doctor assumed that the patient was just having a panic attack – right up until the time of cardiac arrest. Apparently, that was enough of a clue that this was more than just anxiety.

A patient suffocating due to anaphylaxis probably IS having a panic attack.

Especially if people can treat the anaphylaxis, but do not believe it is a real breathing problem. While we should not automatically give epinephrine to patients with panic attacks, we do need to be able to tell the difference between them.

Few of these patients received epinephrine before cardiac arrest.

Waiting for cardiac arrest is waiting a little bit too long to start treatment with epinephrine – we were going to do it anyway as a part of one of the cardiac arrest algorithms.

In order to be less likely to withhold appropriate epinephrine, we should consider titration of epinephrine by infusion –