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

02/10/2011 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs) and at Research Blogging.

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When I wrote Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study – abstract, I was only looking at the abstract. Now that I have seen the entire paper, I have not seen anything weaken the results of the study. There are plenty of points to discuss.

On the EMS Research Podcast Harry Mueller, Patrick Lickiss, Dr. Bill Toon, and I discuss this paper. In about half an hour, we go into the details. Here I will present the highlights. First, go listen to the podcast. Prehospital Needle Thoracostomy: EMS Research Episode4

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During the podcast, I suggested that Dr. Blaivas is a radiologist, or some other specialist in imaging medicine, as opposed to being an emergency physician. That is not correct. Dr. Blaivas is Professor of Emergency Medicine in the Department of Emergency Medicine at Northside Hospital Forsyth in Cumming, Georgia. Dr. Blaivas is also either the world’s first or second emergency ultrasound fellowship graduate. Therefore he is very well qualified to examine all aspects of emergency medicine and ultrasound.

Let’s look at the paper.

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An unstable trauma patient who is not oxygenating well or is hypotensive and has decreased breath sounds unilaterally on auscultation may be assumed by paramedics to have a PTX.2 Not unreasonably, with lack of a more definite way to rule in or rule out the presence of a PTX, needle thoracostomy is opted for to relieve the tension that is assumed to be present.[1]

Previous experience and this study lead me to the doubt this not unreasonable conclusion.

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In the prehospital setting where external noise and distractions may be overwhelming, release of air is frequently not audible.[1]

This focus on decreased breath sounds may be one of the important factors in the misdiagnosis of tension pneumothorax.

How many medics are good at assessing lung sounds?

How many medics can tell the difference between the diminished lung sounds that are indicative of a tension pneumothorax and the diminished lung sounds that are consistent with any of the normal variations of lung sounds?

I would also change part of a sentence –

In the prehospital setting where external noise and distractions may be overwhelming, release of air is frequently not audible imaginary.

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Typically, in such critically ill patients, the chest tube is placed before review of a chest radiograph to confirm that the tension PTX has improved. The natural assumption is that regardless of whether a PTX was present, proper penetration of the chest wall would lead to a PTX even if it were not originally present.[1]

Should any doctor be using this logic to decide to place a chest tube without assessing the patient?

Should any doctor be placing a chest tube without assessing the patient?

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However, if the needle did not penetrate the lung and no PTX was initially present, a chest tube could be avoided.[1]

In the absence of a pneumothorax, a chest tube could should be avoided.

What justification is there for placing a chest tube in a patient with no indication for a chest tube?

Maybe the needle is in the chest because the medic has really scary IV skills. In this study, at least a quarter of the medics treating these patients (unless some are repeat offenders) have really scary needle decompression skills.

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The main outcome measure was whether a PTX was present. The secondary outcome measure was whether a PTX developed after catheter removal.[1]

There does not appear to be any discussion of whether a pneumothorax developed after catheter removal.

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Physicians performed the ultrasound examinations during the secondary survey. Chest radiographs were obtained immediately after the ultrasound examinations. Examiners were not blinded to physical findings or on which side needle thoracostomy was performed.[1]

blinding would have been nice, but this study seems to be more to demonstrate the concept that needle decompression may not even produce a simple pneumothorax. This can be left for a later study.

It would also be nice to follow up on the patients to find out if any showed any of the no pneumothorax patients showed any signs of pneumothorax later on, which could cast doubt on the ultrasound findings.

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A total of 57 patients were enrolled in the study over a 3-year period. Fifty-six patients had 1 needle thoracostomy performed, and 1 patient had 3 needle thoracostomy procedures on the same side for hypotension and persistent unilateral decreased breath sounds.[1]

It should not surprise anyone that the patient with the multiple stab wounds 3 attempts at needle decompression did not have any kind of pneumothorax.

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A tension PTX is a life-threatening process that must be treated immediately either through needle thoracostomy or tube thoracostomy. Despite frequent use of chest radiography on patient arrival to emergency departments, many PTXs are initially missed.[1]

It seems that a lot is missed.

Needles miss lungs.

Medics miss the absence of a tension pneumothoraces.

Doctors miss the presence of pneumothoraces.

If there is an important point to this, maybe it should be that we all need to improve our assessment for pneumothoraces and be more conservative in our treatment in the absence of unmistakable signs of a tension pneumothorax.

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The combination of unilateral decreased or absent breath sounds with instability is justifiably interpreted as the presence of a PTX. There is no way to verify or refute such a finding.[1]

Maybe.

Maybe not.

Should we assume that a tension pneumothorax is subtle?

I don’t think so.

Why do we teach about tension pneumothorax as if it is the same as an easily missed simple pneumothorax?

I think it is because we don’t realize just how unsubtle a tension pneumothorax is.

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This study had several limitations. The first was the small sample size. Second, the sonologists were not blinded to the side on which needle decompression was attempted. Third, it is possible that some patients did in fact have a PTX that was completely relieved by needle decompression, and no more air leaked after catheter removal. Thus, the CT scan would not show even a trace PTX. Although this is possible, it is clinically very unlikely.[1]

There are limitations, but are these results consistent with what we know about the shortcomings of EMS education and understanding of infrequently done procedures?

Absolutely.

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Click on the image to make it larger.

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From this study we cannot tell if the number that should be in the place of the double question marks is 42. Maybe it is 32. Maybe it is 22. Maybe it is 12. Maybe it is 2. Maybe it is zero. We don’t know and this study cannot tell us, which is not a fault of the study.

The same problem exists for trying to figure out the number that should be in the place of the single question mark.

We know that of the patients treated for claimed tension pneumothorax, 26% were treated by paramedics so poorly that the needle never even made it to the lung.

Should we assume that all of the patients treated with needles that actually reached the lung did have tension pneumothoraces?

There is nothing in this paper to suggest that.

There is no good reason to assume that all of the medics who missed the diagnosis also missed the lung. 26% missed the lung and missed the diagnosis.

It is reasonable to assume that some of the medics missed the diagnosis, but used a long enough needle to hit the lung. What we do not know is how many of those who hit the lung with a needle missed the diagnosis.

Another possibility is that the patient had a pneumothorax, most likely a simple pneumothorax, and the medic missed the lung with the needle, but since it was not a tension pneumothorax there was no dramatic deterioration of the patient. The needle decompression would be no more indicated for these patients than for those without any pneumothorax.

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Also covered at EMS Research Podcast Episode 4 at 510Medic.

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Footnotes:

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[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]

Free Full Text from J Ultrasound Med.

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Blaivas M (2010). Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine, 29 (9), 1285-9 PMID: 20733183

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Filed Under: Clinical Discussion, Critical Judgment, EMS Research Podcast, Research, Rogue Medic

Some Food For Thought

11/04/2010 by Adam Thompson, EMT-P 1 Comment
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Some food for thought…

Controversial evidence & some reasoning.

Nitroglycerine is Contraindicated With Tachycardia?

-       BP = Cardiac Output (CO) x Systemic Vascular Resistance

-       CO = Stroke Volume x Heart Rate

An acute coronary event does not cause tachycardia.  Tachycardia (without exertion) is almost always a result of decreased stroke volume.  Stroke volume is dependant on venus return.  So if stroke volume is down, and your body is trying to maintain normal cardiac output, so it may maintain a normal BP, the heart rate may be increased.

If the patient does not have pulmonary congestion (edema), nitro should be withheld if the patient is tachycardic.  This is because the patient may be preload dependant as a result of dehydration, or some other hypovolemic condition.  The tachycardia will most likely be compensatory, and the nitro will worsen the patients condition.

But anxiety can cause tachycardia…

Then console your patient and see if the tachycardia persists after they are calmed.  If the tachycardia seems to accompany anxiety then nitrates may be acceptable.  Be very weary of persistent tachycardia, whether they are anxious or not.

Patients Experiencing a Heart Attack Don’t Need O2?

Oxygen has recently shown to be much less benign a treatment than it was once thought to be.   Hyperoxia leads to increased morbidity and mortality in stroke patients, post-arrest patients, head trauma patients, and it has most recently been discovered that hyperoxygenation may lead to poor outcomes in patients experiencing an AMI.

Why?

The answer isn’t so easy to understand.  First of all, the research is still new.  Just understand that these patients are not generally suffering from hypoxia.  They are suffering from ischemic heart tissue, more specifically—myocardium.  If their oxygen saturation is sufficient, than no additional O2 should be supplemented.  Reasoning includes an elaborate explanation regarding free radicals.  O2 is a free radical and may be toxic, leading to residual oxidative stress.  This causes increased damage.  Use of oxygen in MI patients questioned by new Cochrane review.

What is the Deal With Morphine?

Morphine is associated with an increase in morbidity when given to a patient experiencing an acute coronary event (an AMI).

Once again, there is no conclusive answer, but researchers from a CRUSADE study have three possible explanations.

-       The first explanation is that patients treated with Morphine exhibit signs and symptoms of heart failure, and are treated as such.  This isn’t really accepted as a plausible cause.

-       The second, more widely accepted explanation is that Morphine masks symptoms of angina without correcting the underlined pathology.  This means that caregivers may be less apt to provide follow-up treatments, procedures, and consults.

-       The third explanation is that Morphine decreases the respiratory drive as well as causing CNS depression.  Increased ischemia has been associated with these side effects, and extended infarction has been linked to Morphine itself.

End point No morphine

(n=40 036)

Morphine

(n=17 003)

Adjusted OR (95% CI)
Death (%) 4.7 5.5 1.48 (1.33-1.64)
Death or MI (%) 7.1 8.5 1.44 (1.34-1.56)
Postadmission MI (%) 3.0 3.8 1.34 (1.22-1.48)

Morphine has bad effects when administered to patients with CHF.

Yes, it is in most prehospital guidelines as a recommended treatment for congestive heart failure.  This will soon change…

The Acute Decompenstated Heart Failure National Registry (ADHERE) conducted a study on patients admitted with CHF who received morphine and yielded important results. There was a five-fold increase in mortality (13% versus 2.4%), a five-fold increase in need for intubation and ventilation (39.7% versus 14.4%), the intensive care unit admission rate was (15% versus 3.0%), and those patients who were admitted had a prolonged hospital stay (5.6 days versus 4.2 days). Although this was an observational study, it has had a major impact on the use of morphine for CHF patients.  We know that morphine causes histamine release and subsequent hypotheses have been made concluding that this may increase catecholamine release. This may be the link to the poor outcomes. Additionally, there is a lack of evidence that morphine is related to any clinically significant preload reduction.

No More Intubations?

There has been a new paradigm shift in the way we think of resuscitation.  This has brought with it, some new terminology—cardiocerebral resuscitation (CCR).  CCR is meant to replace CPR, or cardiopulmonary resuscitation.  The focus is shifting from the lungs, or pulmonary system, to the brain, or cerebrum.

There have been suggestions from the result of much research, advocating CCR for witnessed cardiac arrest, and CPR for primary respiratory arrest.  This makes perfect sense, considering the pathologies.  Overall though, there has been much more success when emphasis has been on chest compressions, as opposed to airway management.

Blind insertion, supraglotic airways are now rapidly finding their way into prehospital cardiac arrest guidelines throughout the country.  The Combitube, Laryngeal Mask, and King LT/LTD are a few of the most common devices being utilized.  The big sell, is the ability to insert these devices without any pauses in chest compressions.

This emphasis on chest compressions comes from research showing the need to prime the pump during the circulatory phase of cardiac arrest.  This basically means that the heart and brain need to be perfused as good as possible up until defibrillation.  Immediate defibrillation is only indicated within the electrical phase; which only lasts for approximately the first five minutes of pulselessness.

Despite the turmoil and mixed opinions about ETI in cardiac arrest, the evidence is clear—survival is better when the main focus is on adequate chest compressions.  By taking the ETI aspect, and all of the complications that accompany it, out of the equation, resuscitation efforts consequently improve.

We haven’t even gone to the extreme yet.  One study has shown that by simply placing a non-rebreather mask on a cardiac arrest victim and providing high-quality chest compressions, they increased neurologically intact survival rates from 15 to 39%.

Remember:  Nearly all-medical research is flawed.  This is one reason why medicine will remain ever changing.  Fortunately the good evidence usually trumps the biased or bad evidence.  No single study should change anything.


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Filed Under: AHA Guidelines, Cardiocerebral resuscitation, Cardiology, Clinical Discussion, Pharmacology, Research

Differential Diagnosis: Headache

11/04/2010 by Adam Thompson, EMT-P Leave a Comment
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Differential Diagnosis: Headaches
By Adam Thompson, EMT-P



Headaches account for a large volume of EMS responses.  Most are benign, but a few could be an early symptom of a life-threatening cause.   It may be beneficial to differentiate between the presentations.  A good history is by far the most useful tool that any clinician has in determining a headache’s malignancy.


Common types of headaches:

  • Tension-type headache
  • Migraine headaches
  • Cluster headaches

Tension-type  the most common type of headache, and yet its causes aren’t well understood. A tension headache is generally a diffuse, mild to moderate pain that many people describe as feeling as if there’s a tight band around their head.It may feel as though muscle contractions are responsible for your head pain, but experts don’t think that’s the cause, which is why this type of headache is generally referred to as a tension-type headache. (from MayoClinic)

Migraine a common type of headache that may occur with symptoms such as nausea, vomiting, or sensitivity to light. In many people, a throbbing pain is felt only on one side of the head. Some people who get migraines have warning symptoms, called an aura, before the actual headache begins. An aura is a group of symptoms, usually vision disturbances, that serve as a warning sign that a bad headache is coming. Most people, however, do not have such warning signs. (from Google Health)

Cluster The term “cluster headache” refers to a type of headache that recurs over a period of time. People who have cluster headaches experience an episode one to three times per day during a period of time (the cluster period), which may last from two weeks to three months. The headaches may disappear completely (go into “remission”) for months or years, only to recur. A cluster headache typically awakens a person from sleep one to two hours after going to bed. These nocturnal attacks can be more severe than the daytime attacks. Attacks appear to be linked to the circadian rhythm (or “biological” clock). Most people with cluster headaches will develop cluster periods at the same time each year — either in the spring or fall or the winter or summer. (from WebMD)


Symptom
A
Tension
B
Migraine
Intensity, Duration and Quality of Pain
Mild or moderate pain intensity
√
√
Severe
√
Duration of headache
30 min – 7 days
4-72 hours
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√
Intense pounding, throbbing and/or debilitating
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Distracting but not debilitating
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Steady ache
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Location of Pain
One side of head
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Both sides of head
√
√
Associated Symptoms
Nausea/vomiting
√
Sensitivity to light and/or sounds
√
Aura before onset of headache such as visual symptoms
√

Table 1

Comparing benign headaches

90% of all headaches are benign.  Tension headaches are muscle-contraction headaches, and migraine or cluster headaches are vascular headaches.  Below is a table of accompanying symptoms with each type.

CHARACTERISTICS MUSCLE-CONTRACTION HEADACHES VASCULAR HEADACHES
Incidence
  • Most common type, accounting for 80% of all headaches
  • More common in women and those with a family history of migraines
  • Onset after puberty
Precipitating factors
  • Stress, anxiety, tension, improper posture, and body alignment
  • Prolonged muscle contraction without structural damage
  • Eye, ear, and paranasal sinus disorders that produce reflex muscle contractions
  • Hormone fluctuations
  • Alcohol
  • Emotional upset
  • Too little or too much sleep
  • Foods, such as chocolate, cheese, monosodium glutamate, and cured meats; caffeine withdrawal
Intensity and duration
  • Produce an aching tightness or a band of pain around the head, especially in the neck and in occipital and temporal areas
  • Occur frequently and usually last for several hours
  • Weather changes such as shifts in barometric pressure
  • May begin with an awareness of an impending migraine or a 5- to 15-minute prodrome of neurologic deficits, such as vision disturbances, dizziness, unsteady gait, or tingling of the face, lips, or hands
  • Produce severe, constant, throbbing pain that’s typically unilateral and may be incapacitating
  • Last for 4 to 6 hours
Associated signs and symptoms
  • Tense neck and facial muscles
  • Anorexia, nausea, and vomiting
  • Occasionally, photophobia, sensitivity to loud noises, weakness, and fatigue
  • Depending on the type (cluster headache or classic, common, or hemiplegic migraine), possibly chills, depression, eye pain, ptosis, tearing, rhinorrhea, diaphoresis, and facial flushing
Image 2 – Click the image above to enlarge
Quickie Definitions of Headaches You Never Knew Existed
  • Weight-lifters: Just like you’d think, this is a headache that occurs after a strenuous weight-lifting regimen.
  • Histamine: A headache caused by histamine overload, from a source such a histamine injection or certain wines.
  • Coital: A headache that occurs suddenly during sex or after orgasm. As if couples nowadays didn’t have enough issues – thankfully, these are very rare and actually occur more often in men.
  • Analgesic-rebound: That medication you’ve been taking for your headaches could now be the underlying cause of new headaches. Removal of the medication is required.
  • Hypnic: This is an oddball headache that awakens people from sleep. Clusters can do this as well but the pain of hypnic headaches are not as intense and are not localized around the eye.
High Priority Symptoms
  • The worst headache someone has ever had
  • Headache with stiff neck (especially with a high grade fever)
  • A headache associated with loss of consciousness or altered mental status.
  • A headache accompanied by severe eye or ear pain.
  • A headache that occurs in an individual who has experienced recent head trauma.
  • A headache accompanied by sudden, disabling pain or convulsions.
  • Headache with parasthesia or paralysis

References:

  • American Headache Society – Table 1

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Filed Under: Clinical Discussion, Education, Neurology

Use of Hypertonic Fluids in Traumatic Brain Injury

10/07/2010 by 510medic 3 Comments
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This post is also published at my blog:

An interesting abstract came across Google Reader just now about the prehospital use of hypertonic fluids in patients with traumatic brain injury.  Before discussing the results themselves, I’d like to point out one aspect of particular note:  The study authors looked at 6 month outcomes.  Compare and contrast this to most of the available cardiac arrest research which is only looking at return of spontaneous circulation (ROSC).  The authors in this study are clearly thinking further down the road.  ROSC in and of itself does not equate to improved patient outcomes.  Perhaps we could start looking at resuscitation outcomes 6 month after arrest when publishing new cardiac arrest guidelines, just a thought.

THE SCIENCE
Time for a little review.  If you remember, there are three types of solutions used in medicine:  Hypotonic, hypertonic and isotonic.  Isotonic solutions like 0.9% “normal” saline have the same concentration of solutes (stuff dissolved in them) as the body.  Hypotonic solutions have a lower concentration of solute and hypertonic solutions have a greater concentration.  What does this mean in the body?  Water (the solvent) tends to move to areas which have a higher concentration of solute (solids).  This tendency of water to  ”even out” concentration creates a force called osmotic pressure.  When blood cells (as an example) are exposed to solutions with different concentrations of solute the following results are typical:

by LadyofHats via WikiMedia

When the cells are placed in an isotonic solution, nothing changes.  The flow of water into the cells is matched by the flow of water out of the cells.  When the cells are placed in the hypotonic solution, water flows into the cells to offset the higher concentration inside, causing the cell to swell and break open.  And finally, when the cells are placed in the hypertonic solution, water flows out of the cells in an attempt to normalize the solution outside of the cell.

APPLICATION IN MEDICINE
So what does this all mean to medicine?  We carry isotonic fluids on our vehicles and routinely use them for fluid resuscitation because we want to increase blood volume without placing unneeded stress on the body’s cells.  This study looked at giving a single 250cc bolus of a hypertonic solution to patient with traumatic brain injury (TBI).   One of the effects of TBI is swelling of the brain or cerebral edema.  The idea of giving a hypertonic solution to a TBI patient makes sense from a chemistry sense; it will keep the fluid from being taken up by the brain tissue because osmotic pressure is keeping the fluid in the blood stream.  Basically a hypertonic solution has a tendency to pull water into the blood stream rather than allowing water to leave the blood stream into surrounding tissues.  Giving a hypotonic solution to a TBI patient would likely increase cerebral edema.

THE STUDY
The authors of the study planned to enroll 2122 subjects who would be given a 250cc bolus of 7.5%saline/6%dextran, 7.5%saline or 0.9% “normal” saline by prehospital  providers.  The study was terminated after 1331 patients when the study had met “predefined futility criteria”.  Not having access to the full article, I’m unaware of what those criteria were.  The results, however, show that there was not a statistically significant change in patient outcomes with regard to which fluid bolus was given.

CONCLUSION
So there you have it.  Prehospital administration of hypertonic fluids does not change six month outcomes in TBI patients.  Hopefully the chemistry review was worthwhile.  If there’s any interest in continuing these types of reviews, let me know and I’d be happy to make it a regular feature.  I also think that the study design, and focusing on longer term outcomes is a beneficial approach to prehospital research.  At the end of the day, getting pulses back on a cardiac arrest patient doesn’t matter much if they don’t leave the hospital and go on to live a healthy life just like an improvement for a period of hours or days for TBI patient doesn’t mean much if their long term outcome doesn’t improve.  What do you think?  Are there any other areas of EMS treatment which could benefit from the study of long term outcomes?

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Filed Under: Cardiac Arrest, Chemestry, Clinical Discussion, Education

NAEMSP Dialog – Pain Management

09/27/2010 by Adam Thompson, EMT-P 2 Comments
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Below is one of my replies within the NAEMSP Dialog Group.

My Take:

Pain management starts with stress reduction and visa versa.  One
common modality that is often overlooked is the use of an ice/cold
pack.  For musculosckeletal injuries, this is often my primary
treatment.

I believe that, in general, all [prehospital] healthcare providers,
including myself are poor providers of pain management.  As mentioned
by the others here, this is all-to-often as a result of those whom
inappropriately seek pain management.  Also, not trusting the
patient’s representation of the severity of pain.  Both should have no
baring in the back of an ambulance.

Maybe the paramedicine curriculum has changed, but I don’t remember
the part of the text book that mentions drug addiction as a
contraindication to pain management.  Dr Bledsoe?

Withdrawal symptoms may be worse than overdose symptoms right?  Well
they are most definitely worse than the symptoms that will present
after a therapeutic level of pain relief is reached.  The most common
symptom there is PAIN RELIEF.

Drug seeker = someone still in pain.

Not that every one deemed a drug seeker really is, but lets consider
the consequences of providing them with what they want.  Many who fall
victim to opiod/opiate addiction do so because of an initial symptom
of pain.  They found relief with the drugs, and found pain when they
stopped taking them.  So when they present to EMS with a complaint of
pain, they probably have pain.  Yes, it may be pain due to the falling
levels of narcotic within their body, but do you know that?  More
importantly, do you care?  They are in pain, and we can treat pain.
This is an extreme argument I know.  The argument against this could
be a straw man built on the basis that this would lead to an EMS pain
relief dependancy, or contribution to the problem.  Until us
paramedics are taught differently, shouldn’t we do what we are
taught?  The complaint is real unless proven otherwise.

If we are in the practice of following the evidence, than we obviously
need to rethink the way we withhold pain management.  And by
‘rethink’, I mean ‘omit’.

Consider the following:

If epinephrine was a schedule one narcotic that was commonly abused,
would you withhold it if an “epi-abuser” presented with anaphylaxis?
The drug abuser is often in more pain than the patient who has never
had an opiate in their system.  We aren’t handing out prescriptions or
giving large doses, we are just getting them to the hospital.

This is just my point-of-view and I am aware of the holes.  Nothing is
absolute and this is no exception.

Adam Thompson, EMT-P
Lee County EMS
EMS Educator – Edison State College
Paramedicine101.com
EMSresponder.com
Lee County, Florida

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Filed Under: Clinical Discussion

A Prehospital Pain Management Discussion at the NAEMSP Site

09/21/2010 by Rogue Medic 1 Comment
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Also posted over at Rogue Medic.

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I would have also posted this at Research Blogging, but this discussion is not the kind of research blog post that they are looking for.

Well, what needs to be said about prehospital pain management?

Drug Seekers.

Fentanyl vs. Morphine.

Fractures dispatched BLS vs. ALS.

Standing orders vs. Mother-May-I?

Nitrous oxide, etomidate, ketamine, NSAIDs (Non-Steroidal Anti-Inflammatory Drugs), relaxation, ice, acupressure, et cetera. If it might be used by EMS for pain, it is fair game for the discussion.

Legal issues – when will the lawyers start going after medical directors/medical command physicians for withholding appropriate treatment/neglect/malpractice?

Pediatric Pain Management by EMS.

And more.

There is a discussion of Prehospital Pain Management on the NAEMSP (National Association of EMS Physicians) discussion site on Google Groups. NAEMSP Dialog. Anyone can read the discussions. They are there to be a kind of reference for people working in EMS. This is what some of the top doctors, administrators, educators, street providers, and even the occasional blogger have to say on a topic.

Here is a summary of the rules on participation:

Trying to facilitate a higher level of discourse on contemporary issues in EMS. Most of the list members are physicians, managers, and educators – along with street level EMTs and paramedics with an interest in academics and policy issues.

Everyone who wants to join the list has to provide their name and affiliation; all posts are reviewed by a moderator before being allowed to circulate; and all posts must be ‘signed’. There is some descriptive language about the Dialog on the home page of the Google Group (http://groups.google.com/group/naemsp-dialog).

Go read. If you want to comment, sign up, but don’t try to push the envelope on what you can get away with. The envelope has already been pushed.

Some familiar bloggers are also participating – Adam Thompson, EMT – P from Paramedicine 101, Tom Bouthillet from Prehospital 12 Lead ECG, Mark Glencorse from Medic999, and a couple of doctors from the EMS Garage – Dr. Bryan Bledsoe and Dr. Keith Wesley. Some of the other top medical directors in the country are participating as well.

.

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Filed Under: Clinical Discussion, Critical Judgment, Heresy, Rogue Medic, Uncategorized

Differential Diagnosis Series – Abdominal Pain (Part 2)

09/15/2010 by 510medic 2 Comments
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This post is the second of two detailing the construction of a differential diagnosis for abdominal pain.  The post yesterday consisted of a review of the relevant history and physical exam for abdominal pain patients.  This article is also posted at my site:  510medic.com

COMMON EMS DIAGNOSES
While many causes for abdominal pain require lab work and diagnostic studies in the hospital environment, there are some common or potentially life-threatening diagnoses that are considering “can’t miss” in the prehospital setting.

APPENDICITIS
Appendicitis, as the name might suggest, is inflammation of the appendix.  Caused by blockage of the entrance of the appendix, the organ swells, eventually bursting and filling the abdominal cavity with infectious material.  The result of an abdominal infection is peritonitis, another life threatening condition.  Traditionally, there are several signs that have been taught to EMS responders to determine if a patient has a probable appendicitis:  fever, rebound, guarding and tenderness over McBurney’s point.  As it turns out, fever is neither sensitive (15-67%), nor highly specific (85%) for appendicitis (1).  As a refresher, this sensitivity means that 15-67% of abdominal pain patients with no fever (a negative finding) will not have an appendicitis.  Needless to say, this number does not inspire a lot of confidence in ruling out appendicitis.  Conversely, 85% of patients with an appendicitis will have a fever (1).  McBurney’s point (halfway along a line drawn from the umbilicus to the iliac crest) is no better,  Tenderness over that point is present in only 50% of appendicitis patients.  Lastly, rebound has a sensitivity of 61% and a specificity of 82% and guarding has a sensitivity of 46% and a specificity of 92% (1).  So what this all means is that a patient with abdominal pain and all of the following symptoms:  fever, pain over McBurney’s point, guarding and rebound tenderness likely has an appendicitis.  What this also means is that a patient can have abdominal pain and none of the other symptoms and still have an appendicitis.

ECTOPIC PREGNANCY
An ectopic pregnancy occurs when an embryo implants somewhere other than the uterus.  Most often, this implantation occurs in the fallopian tube and can cause a rupture as the pregnancy progresses.  This obviously represents a significant threat to the life of the mother.  As ruptured ectopic is the leading cause of pregnancy-related death during the first trimester (2), it is important to keep a high index of suspicion, since a patient may not yet know she is pregnant.  To this end, any female patient of child-bearing age presenting with abdominal pain, syncope, hypotension or vaginal bleeding should be considered for a possible ruptured ectopic.  Pain from a ruptured ectopic pregnancy will typically present in the right or left lower quadrant (depending on which side the pregnancy implanted) and may present with profound hypotension.  Ultimately, clinical findings cannot effectively  rule out ectopic pregnancy and an in-hospital ultrasound is needed (2).

PANCREATITIS
Pancreatitis is inflammation of the pancreas occurring in either chronic or acute forms.  Chronic pancreatitis can result from alcohol and illicit drug abuse and, as such, is more often seen in the prehospital setting.  Most of the actual diagnostic work for pancreatitis takes place in the in-hospital setting.  Lab values are particularly helpful including pancreatic function tests and, of course, the ever-present abdominal CT (1).  In the prehospital setting, most of the leg work goes towards history-taking.  Patients with epigastric pain, often radiating to the back, with associated nausea and vomiting and a history of chronic alcohol abuse who have been ruled out for cardiac and respiratory causes should be considered for pancreatitis (1).  Additionally, a history of pancreatitis diagnosis and a comparison of the presenting symptoms to the historical symptoms is helpful.

BOWEL OBSTRUCTION
As the name indicates, this condition occurs when something obstructs the passage of fecal matter through the bowels.  This condition can result from chronic constipation, foreign object, or conditions like cancer or polyps.  Over half of the cases of large bowel obstruction result from the presence of cancer (1).  Patients generally present with episodes of increased pain during which bowel sounds are notably louder (even audible without a stethoscope).  The patient may present with abdominal distention (89% specific), previous abdominal surgery (94% specific) and constipation (95% specific) (1).  While these findings are fairly specific (positive findings rule in large bowel obstruction), they are relatively insensitive (a negative finding does not reliably rule out large bowel obstruction).  Making up 80% of bowel obstruction cases, small bowel obstruction is most often caused by post-operative adhesions (70%) (1).  For the purposes of the prehospital community, large and small bowel obstruction present with essentially the same findings in the history and exam.  Field treatment of bowel obstruction includes fluid resuscitation and pain management.

MESENTERIC ISCHEMIA
The small intestine is supplied with blood and nutrients by the mesenteric artery.  When this artery does not provide adequate circulation, ischemia of the small bowel can result.  While it can be caused by hypotension from hemorrhage in trauma (resulting in the “golden hour” – but that’s another post), the disease process here results from a clot blocking blood flow.  Other than abdominal pain, there are not many physical findings in EMS which can aid in a differential diagnosis of mesenteric ischemia.  If advanced, ischemia may result in decreased bowel sounds.  Often, patients will complain of pain much more severe than their physical finding would indicate (1).  A thorough history will serve the practitioner in this diagnosis.  Patients at high risk for clotting (history of atrial fibrillation, CHF, bed confinement, and recent surgical procedures) should be considered high risk for mesenteric ischemia (1).  Since the presence of mesenteric ischemia can be so life threatening, rapid transport should be considered if this disease process is considered likely.

CHOLECYSTITIS
Hopefully by this point we’re all on board with “-itis” meaning inflammation.  In this case we’re talking about the gall bladder and inflammation and pain specific to it.  The inflammation in question generally results from a prolonged blockage of the common bile duct, often resulting from gall stones.  The pain from cholecystitis is found in the right upper quadrant 54% of the time and in the epigastric region 34% of the time.  The pain generally comes and goes and is often cramping in nature,  radiating to the back, flank and chest (1).  For this reason, it is important to determine where the pain started before radiating and also to perform a 12 lead ECG for abdominal pain patients.

ABDOMINAL AORTIC ANEURYSM
An aneurysm is an out-pouching from an artery caused by a weakening of the arterial wall (see my post about CVA for some images of a cerebral aneurysm; same idea, different location).  In the abdomen, pain can be caused by an aneurysm of the abdominal aorta, a life-threatening condition requiring rapid assessment and treatment.  It is important to note that ultimately, the physical exam cannot totally rule out AAA from consideration.  One of the most important findings in the patient examination for ruling in AAA is orthostatic vital signs.  Since the patient often will not have large quantities of emesis or diarrhea, dehydration is ruled out as a cause of abnormal vital signs. A history of GI bleed symptoms (or lack thereof) will rule in or out that diagnosis as well. The classic presentation of AAA is historical hypertension, presenting with constant, severe abdominal pain, pulsating mass in the abdomen and profoundly positive orthostatic vital signs.  It is important to note, however, that for symptomatic AAA, a palpable mass is only present in 18% of patients (1).  For a ruptured AAA, the treatment is surgical.  Think of this as a trauma patient; the speed with which a patient can bleed out is staggering.  In this case, C3 transport is obviously indicated.

CONCLUSION
Abdominal pain is a frequent call for many EMS responders.  Given the breadth of possible causes, it is important for practitioners to keep a high index of suspicion for life-threatening causes.  Performing a thorough physical exam and history on patients with abdominal pain (even chronic ones!) will help to ensure that “must catch” diagnoses are caught.  Do your patients a favor and make sure that you give them the benefit of the doubt, particularly with a complaint as complex as abdominal pain.

CITATIONS

1 – Stern, Scott; Cifu, Adam; Altkorn, Diane. Symptom to Diagnosis:  An Evidence-Based Guide. New York:  Lange Medical Books, 2006.

2 – Lozeau, Anne-Marie; Potter, Beth. Diagnosis and Management of Ectopic Pregnancy. Am Fam Physician. 2005. 72(9): 1707-14.

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Filed Under: Assessment, Clinical Discussion, Medical Emergencies

Differential Diagnosis Series – Abdominal Pain (Part 1)

09/14/2010 by 510medic 3 Comments
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This post is the second in a series detailing the differential diagnosis process.  The first article reviewed the basics of differential diagnosis and this and subsequent posts will look at the process for specific complaints which frequently present to EMS.  This post is the first of two detailing the construction of a differential diagnosis for abdominal pain.  This article is also posted at my site:  510medic.com

INTRODUCTION
You are dispatched to a private residence 30 minutes before the end of your shift for abdominal pain.  What goes through your mind en route?  Aside from the obvious frustrations of course.  What symptoms do you think about on the way?  What possible diagnoses do you consider?  What concerns do have about the patient?

Abdominal pain represents one of our frequent calls in EMS. It is also one of the hardest complaints to diagnose.  The abdomen houses many organs, any of which could cause pain, and abdominal pain can be a symptom of serious conditions including cardiac disease and pneumonia.

DIFFERENTIAL DIAGNOSIS REVIEW
As discussed in the first article in this series, differential diagnosis is the method of evaluating data from examination and assessment to construct causes for presenting complaints.  An initial list is constructed based on the complaint or body system involved.  This list is narrowed down by findings that move the index of suspicion to the point that you are comfortable either treating or discarding that cause.  The usefulness of a test is quantified by specificity and sensitivity.  A positive result in a highly specific test means it is likely a patient has a certain disease.  A negative result in a highly sensitive test means it is likely that the patient does not have a certain disease.  Tests and assessments continue until your index of suspicion crosses the threshold to treat or ignore and you move to the next potential cause.

CONSTRUCTING A DIFFERENTIAL FOR ABDOMINAL PAIN
In building a list of causes for abdominal pain, the provider considers three important aspects:  the specifics of the pain, the patient’s history and the findings during the physical examination.  When reviewing the patient’s pain, the PQRST mnemonic (P – Provoke/Palliate, Q – Quality, R – Radiation, S – Severity, T – Time) can help to ensure than nothing is missed.  These findings, along with the location of the pain, can help construct a list of causes.  For instance, upper abdominal, or epigastric pain can be caused by the organs in that area:  the pancreas, gall bladder and stomach; though sometimes epigastric pain can result from a heart attack.  Knowing which organs are where is important because, for instance, pain from an appendicitis is likely to occur in the right lower quadrant so choosing that as a differential diagnosis for left upper quadrant pain could be a dangerous mistake.

Abdominal Organ Locations - via Flickr

Along with information about the patient’s pain, you should take a detailed history from the patient.  Knowledge of associated symptoms can aid in the construction of a differential diagnosis.  Some historical findings include:

  • Nausea/Vomiting
  • Diarrhea
  • Constipation
  • Change in oral intake
  • Blood in the stool/urine
  • Fever/Chills

By asking these questions, you are able to know the time frame of the symptoms and the organs or body systems affected.

In addition to symptoms associated with abdominal pain, it is vital to ask about the remainder of their medical history.  Particular attention is paid to respiratory symptoms and any cardiac history as abdominal pain may be a presenting symptom in both an acute myocardial infarction and pneumonia.  Lastly, the patient’s sexual/reproductive/menstrual history should be noted and any alcohol or drug usage.

The next step in the diagnosis of abdominal pain is the physical exam beginning with vital signs.  In addition to the standard set of vitals, consider checking for positive orthostatic changes (a drop in blood pressure and an increase in heart rate when moving from lying to sitting and sitting to standing).  Positive orthostatic findings include a systolic blood pressure drop of 20 mmHg or a heart rate increase of 20 BPM.  Care must be taken with patients on heart rate control medications (like Atenolol) because their heart rates cannot increase during times of shock.

Continuing the physical examination, the practitioner performs a cardiac and respiratory exam including 12 lead ECG, lung sounds and heart tones.  Since life threatening conditions like acute MI and pneumonia can present as pain referred to the upper abdomen or epigastric region, it is important to rule out the presence of these conditions early in the construction of a diagnosis.

Finally, the physical exam proceeds to the actual hands on assessment.  The patient is assessed through visual inspection of the abdomen, auscultation to check for the presence or absence of bowel sounds and palpation using first light pressure then deeper pressure.  During the palpation phase, it is important to talk to the patient to distract him and to work towards the region where the complaint of pain exists.

CONCLUSION
Based upon specific findings during the history and physical examination, the practitioner should be able to determine the underlying cause of the patient’s complaint.  In tomorrow’s post, we will present a review of some of the common causes of abdominal pain and which specific findings may indicate an underlying cause.  Stay tuned!

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Filed Under: Assessment, Clinical Discussion, Medical Emergencies

Learn It: Angioedema

09/05/2010 by Adam Thompson, EMT-P 5 Comments
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Angioedema


Sometimes referred to as Quinke’s Edema, angioedema is that swelling we see that is most apparent around the mucosal areas of the face.  Consider Hives as swelling on the surface of the skin, and angioedema as swelling beneath the skin.  
The most common cause of this type of swelling without the presence of Hives is hypersensitivity to ACE inhibitors.  
ACE = Angiotensin converting enzyme.  This converts angiotensin one into angiotensin two.  
ACE inhibitors block ACE.
Bradykinin is a peptide that has a role with all forms of angioedema.  It is a potent vasodilator that increases permeability and allows the accumulation of fluid within the interstitial space.  
ACE is one of the main ways that bradykinin is degraded.  So when we inhibit the production of ACE, we are then inhibiting the degradation of bradykinin.  We then have this run away peptide and subsequent swelling.  
Many patients that suddenly present with severe angioedema have been taking ACE inhibitors, such as lisinopril, for a long period of time.  They may have never had any issues before, but out of no where have this severe reaction.  This type of reaction is most common in the African-American population, but may occur in anyone.  
There are other types of angioedema, including the traditional allergic reaction.  Those are more well known and prepared for.  
Treatment

As you can see from the pictures above, swelling may be within the oropharynx.  This can cause an airway obstruction, and aggressive airway management should be advocated.  
This patients may be obtunded and snoring as you enter the scene.  They have been confused for diabetics, or acute coronary syndrome patients due to their initial impression.  
It is common for these patients to undergo cricothyrotomy due to complete glottic obstruction.  Moving quickly is imperative to prevent severe hypoxia and cardiorespiratory arrest.
The usual drugs used for anaphylactic reactions are indicated.
- Epinephrine to reduce the vasodilation.  
- Crticosteroids & antihistamines.  
So the next time you run on a patient that is presenting with swelling in the absence of hives, think angioedema, and act fast!


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Filed Under: Clinical Discussion, Education, Pharmacology, Toxicology

Research: Prehospital Thrombolysis

08/09/2010 by Adam Thompson, EMT-P Leave a Comment
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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

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Filed Under: Cardiology, Clinical Discussion, Research
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