Showing posts with label Research. Show all posts
Showing posts with label Research. Show all posts

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



ResearchBlogging.org

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

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.

Drug Shortages Affect Those Still in the Dark Ages – Furosemide

ResearchBlogging.org

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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Drug Shortages Affect Those Still in the Dark Ages – Lidocaine

ResearchBlogging.org

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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Research: Management of the Airway in the Trauma Patient

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.

Research: Management of the Airway in the Burn Patient

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

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

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.  

2010 AHA Updates




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.    

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





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


.

Prehospital use of analgesia for suspected extremity fractures




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]



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