Evaluation of the Canadian C-Spine Rule Continues

Posted by Patrick Lickiss on Jul 27, 2011 in Assessment, General, Research, Treatment | 2 comments

In an article published in February in the BioMed Central of Emergency Medicine (an OPEN journal by the way, not charging $85/article!) a study protocol was laid out for the next phase in the evaluation of the safety of the Canadian C-Spine Rule (CCR).  The full text of the article may be found here (PDF link).

For those not familiar, the CCR is a spinal clearance tool which is basically a cross between the State of Maine and the NEXUS criteria you’ve likely seen physicians use in the ED.  There’s a nice flow chart in the article, but the basics are as follows:

• Does the patient have a high risk factor indicating immobilization?
  • Older than 64 years
  • Dangerous mechanism
  • Numbness/tingling
• Does the patient have one low risk factor?
  • Minor rear-end MVC
  • Ambulatory on scene
  • No neck pain when asked
  • No neck pain with palpation
• Can the patient rotate their own head, left and right, to 45 degrees, regardless of pain

I really like this technique because it just makes sense:  Do they have any big things to worry about?  No.  Do they have something which indicates they’re uninjured? Yes.  Can they move their head? Yes.  Fantastic, don’t c-spine!

A BRIEF HISTORY OF THE CCR
The researchers in Canada have clearly been doing their due diligence.   This project has been on going, in one form or another, for the past 10+ years.  The CCR was first written about in 2001 and was compared at the time to both the standard NEXUS exam and radiological results.  Since then, the procedure has been validated amongst physician, ED triage nurse and paramedic level practitioners.  During the phase I and II trials, the CCR demonstrated a 99.7% sensitivity ^[1].

The researchers have since implemented the protocol amongst physicians in  multiple hospitals and are studying implementation amongst ED triage nurses as well.  One line in the article really stuck in my head after reading it:  ”While we hope to demonstrate that ED triage nurses can safely remove patient’s cervical immobilization devices, it would be significantly more valuable if we could empower the paramedics to selectively forgo immobilization in the first place, and avoid great discomfort to patients.” ^[1] Simply put, I love this idea!  If we have access to a tool which can benefit our patients, why don’t we give it to everyone involved in patient care, so that we can significantly benefit our patients more often!

Additionally, I love the idea of standardizing something like ruling out spinal immobilization across all levels of care from pre-hospital to in-hospital.  The main thing holding this article/study back from being one of the most ground breaking in EMS is the actual statement that spinal immobilization is not, in fact, beneficial and actually harms our patients.  But that might be asking too much.

At any rate, check out the article and stay tuned, the idea of standardizing care across practitioner levels is an interesting one that bears more reflection.

ARTICLE CITED
[1] - Vaillancourt C, et. al: “Evaluation of the safety of C-spine clearance byparamedics: design and methodology”. BMC Emergency Medicine 2011 11:1.

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Pediatric Poisoning Refresher

Posted by Patrick Lickiss on Jul 13, 2011 in Assessment, General, Research, Treatment | 2 comments

While browsing through recent journal articles, I came across a retrospective study published by the University of California at San Diego Emergency Medicine Department ^[1]. Looking back at eight years worth of EMS documentation (this is one of the limitations of a retrospective study) the researchers attempted to quantity particular information about pediatric poisonings in that time period.  I say that this is a limitation of a retrospective study because the validity of the research relies on the quality of documentation performed before the study was designed.  This can prove to be time consuming and may not yield useful results.

THE FINDINGS

There were more than 40,000 paramedic transport calls for patients 5 years and younger over the study period; 996 (2.5%) of these calls had the chief complaint of poisoning. Of the calls classified as poisonings, 38% involved a 1-year-old and 35% involved a 2-year-old. Fifty-six percent of these poisonings involved either prescription or over-the-counter medications. An additional 16% were due to household cleaners. Eighty-eight percent of all calls were classified as mild in acuity, with 13% of poisoning calls for children under a year of age classified as moderate or acute; 50% of moderate or acute poisoning calls were to children 2 years of age. July and March were the months with the highest incidence of poisoning calls. The fewest calls were received on Saturdays and Sundays^[1].

There are a few items of interest in these findings.  First of all, the vast majority (over 70%) of poisonings take place with patients 2 years old and younger.  It seems like a lot of presentations in that population should including poisoning as a potential differential diagnosis, particularly if you are struggling to find a cause for the symptoms.  Next, the majority of poisoning calls for pediatrics involve medications.  Keep in mind that therapeutic effects in adults are potentially fatal in pediatrics.  This is especially true with regards to medications targeted at the cardiovascular system like digoxin and beta-blockers.  Finally, “moderate” or “acute” poisonings were more likely to occur with patients two years of age.  This is logical as these patients are becoming more active and mobile.  When responding to patients in this age group (for other calls, not for poisonings) take a quick look around on scene and see if there are medications or household cleaners in easy reach of children.  This is the perfect opportunity to provide some education to the family, particularly if you’re not the primary caregiver.

NATIONAL STATISTICS
According to the American Association of Poison Control Centers,  over 52% of poisonings in 2009 occurred in patients aged 0-5 years.  Since 2006, the pediatric ingestion of analgesics has seen a particularly marked increase ^[2].  According to the CDC, children are twice as likely to be seen in the Emergency Department for medication poisoning as they are for poisonings from household cleaners ^[3].

ACTIONS WE CAN TAKE
We discussed earlier about maintaining an elevated index of suspicion for poisoning in pediatric patients.  We also discussed gently providing education to caregivers when an unsafe situation is discovered on scene (though not necessarily during a response for poisoning).  What about treatment options?  Poison Control is a valuable resource and every EMS practitioner should have the number in his or her cell phone.  Poison Control is staffed by medical providers who are able to provide you with valuable information, even if you do not know the exact toxin which has been ingestion.  Often, the individual answering the phone will be able to determine the substance based on partial labels, color, uses, etc.  I have had excellent luck with identifying myself as a paramedic on scene of a 911 call after the line is answered.  I am often transferred to a pharmacist right away and have been able to get treatment suggestions as well as findings (including ECG changes) to watch out for.  After that, it’s as easy as contacting my base hospital, letting them know that I contacted poison control and getting an order to treat as suggested by the pharmacist.

I encourage everyone reading this to stop for a moment and put the following number in your phone:  (800)222-1222.  You can call that number from anywhere in the U.S. and you will be connected to your local poison control center.

So how about it?  Have you used Poison Control on duty?  What about off duty?  What was your experience like?  Are you taught about using Poison Control during annual training?  Let me know in the comments.

CITED ARTICLES
[1] - Vilke GM: “Pediatric Poisonings in Children Younger than Five Years Responded to by Paramedics”. J Emerg Med 2011 Jan 5, [Epub ahead of print].

[2] – American Association of Poison Control Centers – 2009 Detailed Statistics (PDF Link)

[3] – Centers for Disease Control and Prevention – Poisoning Factsheet

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AHA Bradycardia Algorithm – Pacing or 12 Lead?

Posted by Patrick Lickiss on Jun 15, 2011 in Assessment, General, Treatment | 7 comments

I was e-mailed a few weeks ago by a friend of mine who had a question about the wording in the AHA guidelines with regards to symptomatic bradycardia and whether it was appropriate to perform a 12 lead ECG before pacing.  He described a patient who presents as hypotensive and diaphoretic with a three lead ECG showing a 2nd degree type II AV block at a rate in the 30s.  The other provider on scene performed a 12 lead ECG before pacing and found that the patient was experiencing an inferior wall MI with elevation in leads II, III and avF.  Excerpted (with permission) are a few lines from that e-mail:

In this case, the 12 lead prior to pacing was very useful, as the hospital used it to make a cath lab decision…but they still took another 12 lead as we switched monitors and before they started pacing again.  ACLS says ‘immediate’ cardioversion or pacing for symptomatic patients.  It doesn’t say anything about getting a 12 lead first.  Had it been my call, I would have been pacing a few minutes earlier and would have never bothered with a 12 lead.  What do you think?

This is a sticky situation.  In reviewing the 2010 AHA guidelines for bradycardia, the statement is made under the heading “Identify and treat underlying cause” to perform a “12 lead ECG if available; don’t delay therapy” ^[1].  Now that seems pretty cut and dry:  If a patient is bradycardic and is symptomatic, treat them as such and figure the rest out later.  I have another thought, however.

What does a patient in symptomatic bradycardia ultimately need?  They need the cause of their altered heart rhythm fixed.  In the scenario presented to me, that cause was a STEMI.  Is a basic ED going to be able to fix that underlying cause?  Nope.  What are they going to do for that patient?  Probably IV fluids, pacing and dopamine, all of which can be accomplished in the back of your ambulance.  If your closest ED happens to be a STEMI specialty center then your destination won’t change regardless of the reading on the monitor.  But what if you have a basic ED 10 minutes away and a STEMI center 15 minutes away?  Suddenly that ECG is potentially pretty important.

In my opinion, one of the most important things we do in the field is make destination decisions.  At the end of the day, our job is to get the patient to definitive care.  The decision of where to take a patient is an important one and cannot be made without thorough assessment.  In this case, I believe that “thorough assessment” includes a 12 lead ECG.  With proper team work, that 12 lead can be performed while someone else sets up pacing.

Another common scenario in the field is whether to give nitroglycerine for chest pain before a 12 lead is performed.  While less emergent than pacing, the thought process is similar.  Why would you perform a treatment that could obstruct your ability to determine what the underlying cause of the patient’s condition is?  This negatively impacts your ability to get the patient to the correct destination.  Tom Bouthillet over at EMS 12 Lead has a great case study about this exact phenomenon.

Again, the decision to pace a symptomatic patient is very different than the decision to administer nitrates for chest pain.  Consider, however, the implication of performing that 12 lead ECG while pacing is being set up, particularly if it may alter your destination decision.  Be sure to consult with your medical director before making treatment decisions like this.  I think it’s a worthwhile conversation for us to have with our directors, what do you think?

CITED ARTICLES
[1] - Neumar RW, et al.: “Part 8:  Adult Advanced Cardiovascular Life Support:  2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation 2010; 122: S729-67.

The Prehospital Shock Index

Posted by Patrick Lickiss on Jun 8, 2011 in Assessment, Research, Treatment | 1 comment

The body is an amazing piece of machinery.  There are compensatory mechanisms and back up compensatory mechanisms, all designed to maintain homeostasis in the event something goes wrong.  Prehospital providers are likely familiar with the response the body exhibits to blood loss.  After experiencing a traumatic event, say a ruptured spleen from a motorcycle accident, the circulating blood volume begins to drop as uncontrolled internal hemorrhage continues.  During this early stage of shock, the body takes steps to compensate for the blood loss, most notably (and measurable) an increase in heart rate.  As shock progresses, and the body begins to decompensate, the heart rate gradually drops and blood pressure soon follows.

In the case of the ruptured spleen (obviously a serious injury requiring surgery and likely a blood transfusion) early recognition of the severity of the patient could guide destination or more rapid transport. In some cases, waiting until the patient becomes hypotensive may be too late to make a proper treatment or transport decision.

THE PREHOSPITAL SHOCK INDEX
In an article published in February of this year^[1], researchers suggested a method to predict the need for large-scale blood transfusion (more than 10 units of red blood cells in the first 24 hours) based on dividing the heart rate by the systolic blood pressure.  The new CDC Field Triage Criteria focus on blood pressure but not heart rate.  Perhaps including heart rate could prevent undertriage of these potential serious, though compensated patients.

DO WE NEED ANOTHER SCALE?
As I discussed in the stroke series, I think that all too often, scales and assessment tools are given to EMS practitioners and can be used, incorrectly, as a substitute for actual learning.  That being said, if you’re interested in the article, the abstract can be found here.  What I find more useful than adding another “tool” to our tool box is to look at the pathphysiology behind the tool.  In this case, the concept is pretty straight forward.

To review:

• Compensated shock: a state where the body uses methods to maintain circulation despite volume loss.  These can include, increased heart rate, constriction of the vasculature and decreased urinary output.
• Decompensated shock: a state where the mechanisms the body uses to maintain perfusion begin to fail.  Includes dropping heart rate, blood pressure and circulation to vital organs.

Obviously the goal is to figure out when the patient is in compensated shock and to do something before he moves to decompensated shick.  Knowing that the mechanisms used to compensate for shock include tachycardia, we should be paying particular attention to all of the vital signs of patients who “should be” hypotensive.

Take our ruptured spleen for example.   The patient walks up to your ambulance complaining of left lateral abdominal pain after a solo motorcycle accident.  The location of the call is far from your normal response zone so it took 25-30 to arrive on scene.  The patient appears agitated.  After performing a rapid trauma exam, you note that the patient is experiencing tenderness with palpation to his left upper abdominal quadrant.  His blood pressure is 138/80, heart rate is 130 and respiratory rate is 26.  Are you concerned about this patient?  Is his heart rate due to stress from his accident or is he in compensated shock?  Is his respiratory rate due to anxiety or is he trying to maintain oxygenation with a diminished circulating blood volume?

What the decision comes down to is this:  Do you have an index of suspicion that this patient experienced an injury which left him volume depleted?  Could this patient’s vital signs be the result of that volume depletion?  Hopefully you don’t need another scale or assessment tool to answer those questions.

CONCLUSION
Interestingly enough, however, the researchers found that patients with a Shock Index of 0.9 or higher (basically patients with a  heart rate near to or greater than systolic blood pressure) where 1.5 times more likely to need significant blood transfusion.  What common sense tells us is a “big sick” trauma patient based on mechanism, assessment and vital signs turns out, in this study at least, to actually be a “big stick” trauma patient.  Score one for common sense in EMS!

CITED ARTICLES
[1] - Vandromme MJ, et. al: “Identifying risk for massive transfusion in the relatively normotensive patient:  utility of the prehospital shock index”. J Trauma 2011 Feb; 70(2): 384-8.

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Field Differentiation Between Ischemic and Hemorrhagic Stroke – Part IV

Posted by Patrick Lickiss on May 13, 2011 in Assessment, General, Treatment | 0 comments

This is part of a continuing series on the field differentiation of ischemic and hemorrhagic strokes.  Check out Part I for the background. Researchers found that atrial fibrillation (discussed in Part II), DBP < 100 mmHg (discussed in Part III) and lack of change in consciousness were associated with ischemic rather than hemorrhagic stroke.  This post will focus on change in level of consciousness and why it might be associated more readily with a hemorrhagic stroke than an ischemic stroke.

INCREASING INTRACRANIAL PRESSURE
After a blood vessel bursts within the brain, blood begins to fill the space surrounding the site.  Since the skull is basically a closed container, this bleeding starts to build pressure.  That pressure can push the brain downward, towards the only opening in the skull, the foramen magnum.

As the brain is pushed down, pressure is placed on the midbrain, above the brain stem.  The midbrain is responsible for sleep/wake cycles, motor control and alertness, among other tasks.  This pressure is responsible for the changes in consciousness associated with hemorrhagic stroke.

So, much like increased diastolic blood pressure, since altered level of consciousness is associated with hemorrhagic stroke, lack of change of consciousness can be associated with ischemic stroke.

CUSHING’S TRIAD
As intracranial pressure increases further, patients can begin to exhibit signs of Cushing’s Triad.  The clinical signs are hypertension, bradycardia and ataxic or irregular respirations.

Because of increased intracranial pressure and the compression of the blood vessels in the brain, the brain experiences ischemia (as a result of hemorrhage confusingly enough).  In order to maintain blood flow to the brain, the body increases blood pressure.  The increased pressure on the brainstem and midbrain begin to interfere with the cardiovascular and respiratory functions of the brain resulting in bradycardia and irregular respirations.

Findings consistent with Cushing’s Triad are significant and concerning.

CONCLUSION
Throughout this series, we have looked at three possible indicators that a patient may be having an ischemic rather than hemorrhagic stroke:  atrial fibrillation, diastolic BP < 100 mmHg and lack of change in consciousness.  This may not affect your destination decision, but it may change how you treat the patient, for example, choosing whether to treat hypoglycemia as well.  Any questions or thoughts?  Please leave a comment.

NOTE: This series of posts is meant to be educational and should not be used as a substitute for existing policy and procedure.  If you are inspired to change how to treat patients, contact your medical director.

Field Differentiation Between Ischemic and Hemorrhagic Stroke – Part III

Posted by Patrick Lickiss on May 6, 2011 in Assessment, General, Treatment | 0 comments

This is part of a continuing series on the field differentiation of ischemic and hemorrhagic strokes.  Check out Part I for the background. Researchers found that atrial fibrillation (discussed in Part II), DBP < 100 mmHg and lack of change in consciousness were associated with ischemic rather than hemorrhagic stroke.  This post will focus on diastolic blood pressure and why a pressure lower than 100 mmHg might be associated more readily with an ischemic stroke rather than a hemorrhagic stroke.

PREVALENCE OF HYPERTENSION
According to the Centers for Disease Control,  1 in 3 adults in the US has hypertension.  Hypertension is known to be a risk factor for stroke which is the third leading cause of death in the US.  A few other facts from the CDC:

• High blood pressure was a primary or contributing cause in 326,000 deaths in the US in 2006
• Control rate among hypertensive patients is 46.6%
• Hypertension is more prevalent in men than women (31.8% vs. 30.3%)
• Hypertension is more prevalent in patients 55 and older
• Hypertension is more prevalent in African American populations

WHAT EXACTLY IS HYPERTENSIVE?
High blood pressure is defined by the CDC as a systolic BP greater than 140 mmHg or a diastolic greater than 90 mmHg.  According to the Mayo Clinic, stage 2 (more significant) hypertension begins at 100 mmHg, likely why this number was chosen by the study authors.

WHY WOULD HYPERTENSION CAUSE HEMORRHAGIC STROKE?
As discussed in Part II of this series,  a hemorrhagic stroke occurs when the vasculature in the brain ruptures causing bleeding.  Chronic, extreme hypertension, as seen in a patient with a diastolic blood pressure greater than 100 mmHg, can weaken the walls of the cerebral vasculature, allowing an aneurysm or outpouching to form.  With sustained elevated blood pressure, this aneurysm can burst resulting in a hemorrhagic stroke.

CONCLUSION
Since high diastolic blood pressure is so closely associated with hemorrhagic stroke, it seems reasonable (and is supported by the study findings) that lower diastolic blood pressure in the presence of stroke symptoms is associated with ischemic stroke.  Think of blood pressure as another tool when building your differential diagnosis for stroke patients but remember to look at the whole picture before making any treatment or destination decisions.  Any thoughts or questions?  Drop me a line in the comments!