Clearing the Cervical Spine with Distracting Injuries

Ah, the “distracting” injury. An utterly subjective and modifiable component of cervical spine clearance in the NEXUS criteria. Is it an isolated finger dislocation? Is it a femur fracture? We’ve all seen patients writhing or stoic in the face of either. And, then, factor in any prehospital analgesia ….

This is a prospective, observational study coming out of the American Association for the Surgery of Trauma evaluating the effects of distracting injury on cervical spine clearance. For their purposes, the following injuries were considered “distracting”:

Skull fracture, >2 facial bone fractures, mandible fracture, intracranial hemorrhage (including subdural hematoma, epidural hematoma, subarachnoid hemorrhage, intraventricular hemorrhage, intraparenchymal hematoma), >2 rib fractures, clavicle fracture, sternal fracture, pelvic fracture, thoracolumbar spine fracture, intra-abdominal injury (including solid organ injury, hollow viscus injury, or diaphragmatic injury), femur fracture, tibia/fibula fracture, humerus fracture, radius/ulna fracture, and hip or shoulder dislocation.

The physical exam consisted of midline neck palpation and, absent any contraindication, active range of motion of the neck in flexion, extension and rotation. The cervical collar could be removed at the discretion of the treating team, but – in classic traumatology fashion – all patients underwent CT of the cervical spine, regardless of exam.

There were 2,929 blunt trauma patients with GCS ≥14, and 222 had cervical spine injuries identified on CT. Of these injuries, 25 were “missed” by the clinical exam. The “good news”: the rate of miss was “the same”, regardless of distracting injury – 0.7% vs. 1.3%. The bad news, of course, is that a normal physical examination missed 11% of cervical spine injuries. One patient whose injury would have otherwise been missed by a negative physical examination underwent operative intervention.

While there is some obvious spectrum bias associated with any observational cohort enrolled at trauma centers, it is still a reasonable estimate of the sensitivity and specificity of the physical examination. Clearly, it’s not bulletproof in the context of multi-system trauma – but, depending on the pretest likelihood of a cervical spine injury based on other presenting features, a distracting injury need not disqualify a patient from clinical clearance.

“Clearing the Cervical Spine in Patients with Distracting Injuries: An AAST Multi-Institutional Trial”

Offener Brief an den ERC

Open Letter to the European Resuscitation Council.

Dear Ladies and Gentlemen,

Since the PARAMEDIC2 Trial was published, the medical community has been actively debating the different aspects of resuscitation in OHCA. Through free online access medical education (FOAM) different authors have been interpreting the results, and commenting on ethical issues.

The German Resuscitation Council (GRC – Deutscher Rat für Wiederbelebung) posted a comment on their Facebook Page on the 13th of August 2018. This is the Link.
I will translate the comment for your benefit, which was written bei Professor Bernd Böttiger, currently the chairman of the GRC, and member of your board, director of science and research.

Last week Wednesday the PARAMEDIC2-Trial, a randomised, controlled trial with adrenaline compared to placebo with 8016 patients with OHCA in Great Britain was posted here. Since there have been many comments, Professor Böttiger has written up some more important facts:

– Adrenaline versus a Placebo was trialled in a “paramedic” only system
– Emergency Doctors were not on scene in Great Britain
– The thirty day survival rate was very very low, at 2,4% and 3,2% – in Germany this rate is 3-4 times higher
– In 2003 Professor Fischer proved in an EU-funded trial in a direct comparison of the cities Bonn and Birmingham that our physician-based system has a 4x higher survival rate than the “paramedic”-system in England
– We, ourselves, could prove that the survival rate doubles through the use of emergency physicians during prehospital resuscitation in a world wide Meta-Analysis

– The trial drug (adrenaline or placebo) was given 21 minutes after the emergency call, although the Ambulance service was on scene very very quickly, in just under 7 minutes (median 6.5 min). The Vasopressor was only used very very late, and we know very well – again from trials: the sooner adrenaline is administered, the better it works. In physician-based systems this happens much faster. One might say: 21 min after the call the the patients were were so dead – as displayed by the very bad survival rates- that the heart could be restarted, but the brain couldn’t be.
– and another thing: only about 70% of the Patients of the adrenalin-trial received an i.v. line, the other 33% received an intraosseous line – and that is usually done only if you cannot establish an i.v. line in a certain time…
– It’s a similar story with the airway management in the adrenalin trial: 71% received an extraglottic airway, and only 30% were intubated endotracheal…
– A high percentage of patients was taken to hospital during CPR…
– SO IN CONCLUSION the most impressive thing in the negative sense was the very very low survival rate – both with and without adrenaline – despite a bystander CPR rate of 60%! How can or should one explain that, other than because of a system, that perhaps can or must be improved greatly?
– So therefore my clear statement: Our OHCA survival is luckily 3-4 times better and if this is the case then we don’t know if adrenaline might help or not in our quite obviously much better outcome-associated system….
– SORRY, I believe if one is really sick, and one’s life is in danger, then a well trained doctor is helpful. That goes for situations in prehospital and hospital settings, and in hospitals doctors are probably helpful…. That’s what I think….
– I therefore plead in favour of our nation wide cooperative ambulance and emergency doctor system which should be in high regard and maintained.
Thank You

There are a number of things I find irritating about this commentary.
I kindly ask if you could elaborate on some points, for example, is the 30 day survival in Germany and the UK comparable, or are there aspects which must be taken into consideration when comparing these numbers?
For instance the low survival rate of the trial could be explained by some 600 Patients having ROSC early, and therefore not being included in the trial and subsequently not being included in the trial results.

Are you aware of reasons which could contribute to the  long time from arrival of EMS until administration of adrenaline? Does the UK use single responder paramedics and could the challenges faced by such a single responder help explain these times?

Mr Böttiger states that an emergency physician on scene will improve OHCA survival rates by 50 to over 200%, can you elaborate on this point?

Mr. Böttiger’s statement has caused confusion and uncertainty inside the German paramedic and emergency medicine community, is this comment an accurate depiction of the current data regarding OHCA and ALS-CPR? If so, will you be recommending introducing doctor-based EMS in all European countries?

Thank you to everyone involved in the ERC and national RCs for your valuable work, in giving providers guidance on the best possible course of action based on evidence. Please help us understand this statement better.

Michael Stanley

Der Beitrag Offener Brief an den ERC erschien zuerst auf #dasFOAM.

Tachycardia and ST Elevation.

This Case was sent from Anonymous.

A middle-aged patient was sent to the ED with tachycardia. He denied any sensation of palpitations, but his heart rate was consistently 150 bpm. The other vitals were normal. He had JVD and swollen legs, but clear lungs and a normal room air oxygen saturation.

He denied all typical and atypical ischemic symptoms. He noted, however, that he had had marked fatigue starting about 5 days ago, but that he was actually feeling much better today.

The initial ECG:

The rhythm appeared to be atrial flutter, but also concerning were the ST segment elevations in I, aVL, V2, and V3, as well as ST depression in the reciprocal inferior leads.

But atrial flutter can alter the baseline such that there is only apparent STE or STD (see example cases below) 

Is this:
1) true STEMI (acute or subacute)?
2) PseudoSTEMI due to the underlying atrial flutter wave?
3) PseudoSTEMI due to old MI (persistent STE after previous anterior MI, also known as LV aneurysm morphology?

The physician's thoughts: This pattern is concerning for anterior wall OMI, specifically a proximal LAD lesion. There are Q waves in V1-V3, suggesting an old anterior MI, but the T waves in V2 and V3 are fairly tall, suggesting some degree of acute ischemia. Also, there are no T wave inversions which would suggest a subacute, evolved, or reperfused MI.

The patient, with an easy smile, again denied any symptoms.

Atrial flutter can mimic the ECG signs of an MI. (For example, see this case, this case, this case, these erroneous computer interpretations, and this case report
.) To clarify the ECG, the emergency physician administered IV metoprolol to slow the ventricular response. However, the patient became borderline hypotensive after this (although still completely symptom-free). A bedside echo was performed:
There is akinesis of the anterior wall, best seen on the parasternal short axis (PSSA) view.
So there is a myocardial infarction.
But is it old or new?
There is no evidence of aneurysm formation on this echo (the myocardial wall is not thin); therefore, it appears to be acute or subacute.

The cardiac catheterization team was activated. The blood pressure dropped precipitously while in the lab preparing for the angio, and the patient was electrically cardioverted. An occlusion of the proximal LAD was then found and intervened on.

The troponin obtained in the ED was almost 10 ng/mL, suggesting a subacute occlusion.

This was recorded next AM:
There are QS-waves with continued ST Elevation with large upright T-waves in V2 and V3

Smith comment:

Is this the so-called “left ventricular aneurysm” pattern? --LV aneurysm can be distinguished by the size of the T-wave, specifically the T/QRS ratio:

--LV aneurysm has a relatively small T-wave, often with some slight (shallow) inversion.

--Acute MI has a large upright T-wave, but may be inverted if reperfused (shallow in the case of Wellens' pattern A; deep in patthern B, which is a later evolution). However, Wellens' waves are preceded by R-waves, not by QS-waves.

LV aneurysm rule: One should especially suspect LV aneurysm, and use the rule, when there are QS-waves in any of V1-V4. A QS-wave means a single negative deflection, without any R-wave or with only a tiny r-wave.

Here is the rule:

If there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is acute MI. If less then 0.36, it is either subacute (over 6 hours) or old.(see references 1, 2). In this case, the T/QRS ratio is largest in V3 at 5/9 = 0.55.

If this were the presenting ECG, you would not want to say that those QS-waves are due to old MI with persistent ST Elevation (LV aneurysm morphology).

But now we are post-reperfusion, so what does the ECG tell us?
That there is persistent ischemia in spite of reperfusion.

This is a bad prognostic sign. The STE and hyperacute T-waves at this point could be either persistent ischemic or re-occlusion. If there had been intervening resolution on the ECG, it would represent re-occlusion. But in this case it was persistently elevated ST segments and hyperacute T-waves. This is typical of "no reflow," which is a result plugging of downstream small vessels by platelet-fibrin aggregates. Read about it here:

Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction (Lancet 1997)

[Alternative explanation for persistently upright T-waves: post-infarction pericarditis (which happens in transmural MI)].

T/QRS ratio to differentiate anterior STEMI from anterior LV aneurysm:

Case by Anonymous, continued

My personal M and M session:
If there is a similar “next time,” I may change my approach.

First, I deferred the echo too long. My initial reasoning was that this was just a rhythm problem, and that checking the Ejection Fraction at a rate of 150 was unreliable, and would be falsely low. Had I done the echo before the metoprolol, I likely would have felt more justified in considering cardioversion first!

Second, in retrospect, cardioversion would have been better than medications, both because his hemodynamics were precarious, and because it would have clarified the ECG interpretation. I delayed cardioversion because the patient looked “too good” for electrical therapy. Furthermore, the patient was likely in atrial flutter for greater than 48 hours, theoretically raising the risk of post-conversion CVA.

But sometimes ST changes will disappear with conversion of atrial flutter to NSR, and urgent angiography can be avoided. Or, in this case, the true ST segment changes will be revealed, and appropriate timing of angiography can be determined.

Smith comment:

I agree. Electrically cardiovert, then re-assess.