A couple of weeks ago Google+ introduced the concept of “communities,” where like-minded individuals can meet up to discuss their common interests. So, with great fanfare, I’d like to formally announce the creation of the ECG+ community!

Click our logo to check out ECG+

We’re already a few posts deep, so check out the cases and comments and please share your own!

Although I’m an ECG-o-phile, I’ve always been reticent to turn The Medial Approach into a “ECG cases” blog. For one thing, folks like EMS 12-Lead and Dr. Smith’s ECG Blog already do that, and quite well I may add. They have giant readerships, and rather than try to match their success with this small blog, I’ve been fortunate that my friends at those sites have graciously posted any of my ECG’s I felt warranted significant dissemination.

On another front, medical discussions on Facebook have taken off over the past couple of years thanks to the creation of great groups and pages like:

• EKG Club
• Rhythm Watchers
• Living in the Emergency Department
• Prehospital 12-lead ECG Blog (EMS 12-Lead’s Facebook wing)
• Tac-Med, LLC

The one downside to having these discussions on Facebook is that there’s no real way to archive, index, and sort out posts. You may vaguely recall a great case of papillary muscle rupture secondary to acute inferior MI that was shared on some Facebook page a year ago, but with new posts daily and no real way to sort through them, it would take a lot of work to find. The conversations we have on Facebook are always interesting and enlightening, but they’re far from permanent.

Which is where Google+ communities come in. I’m far from familiar with how this is all going to shake out, but after a little reading on the new feature it seems like the best social media option for just this sort of thing. In addition to all the benefits that come with Facebook groups or pages, tracings, cases, and discussions will all be indexed, searchable, and discoverable. It’s a much more permanent, professional, and user-friendly way for us to learn, share, and grow.

So, without further ado, come check us out and let me know what you think!

The post The ECG+ Community appeared first on The Medial Approach to Emergency Medicine.

So here’s the case: You’ve just run an 12-lead on a patient experiencing chest pain and recognized ST-depression in leads V2-V4. Being some manner of an astute provider, your next move is to set up posterior electrodes for leads V7-V9 to confirm the hidden STEMI. You’re about to press the print button, but suddenly your monitor dies. How can you confirm that this patient is experiencing an isolated posterior STEMI and would benefit from immediate PCI as opposed to medical management?

Click image to enlarge. Click here for source. Courtesy of LifeintheFastLane.com.

Hopefully you surmised from that title that I think you should look at V6. And not just look at it; really scrutinize it.

It’s a simple enough idea, but I don’t see it get a lot of discussion. Aside from doing the flipped-and-backwards trick when looking at V2-V4, V6 is the closest thing we have to a true posterior lead on the standard 12-lead. It makes sense that if you’re placing V6 correctly, it should be awfully close to where V7 would end up. It’s also uniquely positioned halfway between V2-V4 and V8-V9, the leads that exhibit the greatest magnitude of ST-depression and ST-elevation respectively during an isolated posterior STEMI.

Because of these two attributes, there’s actually two “V6 signs” that I’ve picked up on:

1. The abnormal V6 sign – a result of changes in V7 affecting V6 next door
2. The normal V6 sign – a result of the ST-deviations in V2-V4 and V8-V9 cancelling each-other out.

So let’s start with the less nuanced and controversial of the two.

The abnormal V6 sign

The “abnormal V6 sign” is any finding of ST-elevation, hyperacute T-waves, or loss of T-wave concavity in V6 when you suspect posterior wall MI because the ECG exhibits ST-depression in the right-precordial leads.

The 12-lead above is a subtle example. Yes, there are changes in the inferior leads as well, but let’s ignore those for now and zoom in on V6…

V6 from the above tracing cropped and zoomed.
Click image to enlarge. Click here for source. Courtesy of LifeintheFastLane.com.

There is a very small amount of abnormal ST-elevation (0.5mm 60ms after the J-point). There is also worrying straightening of the upslope of the T-wave, where it has started to lose its upward concavity and “smile.” I actually find it easier to appreciate these changes zoomed-out and looking at the full 12-lead.

It’s tempting to dismiss these minor abnormalities, but let’s see what V7-V9 would show…

The posterior leads exhibit clear ST-elevation, clinching the diagnosis of posterior STEMI.
Click image to enlarge. Click here for source. Courtesy of LifeintheFastLane.com.

Here’s a similar tracing from the posterior MI section of an EMJ review article looking at the ECG in myocardial infarction:

Again there is very minor ST-elevation and straightening of the initial portion of the T-wave in V6, extending to V5.
Click image to enlarge. Click here for source.

More tracings? I’m always glad to oblige…

The T-waves in V6 feature a hyperacute morphology.
Click image to enlarge. Click here for source.

Here’s a tracing from my last post that partially inspired this one…

Leads V2-V6, zoomed and cropped. Note the abnormal morphology of the T-wave in V6.
Click image to enlarge. Click here for source.

Here’s the tracing that first piqued my interest in V6. In this case the lead labelled V6 was actually located at V7 because of the presence of a defibrillator pad, but that slight position change resulting in drastic ST-elevation really got me thinking about how close V6 is to the posterior leads.

V6 is actually located at the position of V7. Click image to enlarge.

And another…

V6 is again abnormal, with loss of concavity and slight ST-elevation
Click image to enlarge. Click here for source.

Here’s one with clear inferior STEMI. There is ST-depression from V1-V4, but elevation in V6 confirms this is secondary to posterior STEMI and not the common misdiagnosis of “anterior ischemia.”

Click image to enlarge.

Another clear inferior STEMI, but V6 clinches posterior extension…

Click image to enlarge. Click here for source.

An extremely subtle infero-posterior STEMI, but V6 is definitely abnormal in the presence of ST-depression from V1-V6.

Click image to enlarge. Click here for source.

Are you noticing a pattern yet?

This is the most subtle V6 of the bunch, but there’s definite straightening of the up-slope of the T-wave, especially in comparison to V5.
Click image to enlarge. Click here for source. Courtesy of EMS12Lead.com

As evidenced in the last tracing, there’s a very fine line between normal and abnormal when you’re looking at V6 during a posterior wall myocardial infarction. In fact, in part II of this discussion I’m going to look much more into the idea of a normal V6 being a significant finding when you suspect posterior STEMI, so look forward to that post soon.

With all the pretty pictures out of the way, let’s get something on the table. This trick isn’t really going to save lives or expose some previously unrecognized secret of electrocardiography, but let me know if it does. It’s just a shortcut I use on suspicious tracings when I don’t have the posterior leads. It’s rather unlikely that your ECG machine is going to kick the bucket on you between strips, but I’ve seen enough tracings where posterior leads were not run for some reason that I end up using it quite a bit.

I could honestly live without the V6 sign by just relying on the more concrete signs of posterior MI discussed elsewhere, especially at Dr. Smith’s ECG Blog and Life in the Fast Lane. Sometimes, however, we all just need a little extra convincing, and that’s where this comes into play. In fact, I could probably just as well call it the “lead III, aVL, or V6 sign” because those other two leads often show similar subtle changes, but in my experience V6 is slightly more useful during truly “isolated” posterior MI, so I’m going with that. Here’s a great “aVL sign” case posted last week by Dr. Brooks Walsh of Mill Hill Ave Command at EMS12Lead.com that proves V6 isn’t the only lead you should be looking at.

Lest I be accused of carelessly putting out information without context, let’s discuss some more of the shortcomings of the V6 sign:

• I just made this up based on the case series that is my experience and study. It has not been previously studied or validated as far as I’m aware. If someone wants to study this (or especially my next topic of the “normal V6 sign,” please contact me.
• It’s just a piece of the puzzle. You need to use this in combination with other ECG findings to make any diagnoses or decisions.
• It’s not even a unique sign, but just a common result of the other findings you see with a posterior wall MI. I’m not being overly creative here.
• As I’ll discuss in my next post, perhaps you should actually expect V6 to be NORMAL during a posterior MI, but this is for those cases when you get lucky.
• ST-elevation in the posterior leads is often focused towards V8 and V9, so it may not always extend out to V7 and V6. This is not even close to being a substitute for running posterior leads.

I’ve already gone on for way too long at this point. Make sure you check out Part II in a couple of days (or tomorrow or whenever I get around to it) for some more tracings and hopefully less reading! And don’t forget to let me know what you think in the comments!

The post Posterior MI Part I – The Abnormal V6 Sign appeared first on The Medial Approach to Emergency Medicine.

I was doing some light reading the other day and stumbled upon this article by R. Shinde et al, entitled Occurrence of “J Waves” in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis. I don’t have access to Pacing and Clinical Electrophysiology, but the authors’ original manuscript is available for free here and can’t be too different from the finished product. In the end I wasn’t too intrigued by their whole J-wave hypothesis, but an ECG in their case study did catch my eye.

Serial 12-leads from a 28 year-old man experiencing chest pain. Click image for source.

In the paper, they describe these ECG’s:

Electrocardiogram (ECG) recorded during pain was unremarkable except for presence of “J Waves” in leads I and aVL (emphasis mine). There was no pain thereafter. However, suspecting ischemia, he was kept under observation. Repeat ECG after 12 hours showed no change. However, the ECG after 24 hours showed positive recruitment in R wave voltage in lead V1 along with ST-T changes in inferior and lateral wall leads. The “J Waves” in leads I and aVL were absent. A diagnosis of true posterior wall infarction was made from the ECG. Serum Troponin-T was 3.5 ng/dL (Normal < 0.05 ng/dL). 2D echocardiographic examination of the heart revealed postero-inferior hypokinesia with an ejection fraction of 40%. Subsequently, he underwent coronary angiography, which revealed complete occlusion of left circumflex coronary artery (LCx) after the origin of the first obtuse marginal branch.

As you may have figured by this point, instead of being “unremarkable,” the initial ECG is quite close to being diagnostic for acute coronary occlusion. Why can I say that? Let’s take a look at some of the precordial leads again.

Leads V2-V6, zoomed and cropped. Click image for source.

Walking stepwise through what we see:

• The R-wave transition starts a little early with a decent sized R-wave in V2, but this could just be normal-variant for a 28 year-old.
• There are abnormally horizontal ST-segments from V2-V5.
• There is a small amount of ST-depression from V2-V5 (0.5 – 1 mm).
• Accompanying the ST-depression, there are upright T-waves.
• There is a good amount of baseline sway complicating things in V6, but the T-wave shape is unusually convex with a slightly high takeoff when compared to V2-V5. This may be an “injury pattern.”
• The other seven leads are otherwise normal.

All of these findings point to one thing: isolated posterior STEMI. You don’t need fancy J-wave recognition to tell you there is an acute coronary artery occlusion. All you need are posterior leads V7-V9.

Here we don’t have them to confirm that they would have shown ST-elevation, but with the standard 12-lead, coronary angiography, and echocardiogram all pointing towards posterior MI, I feel quite confident that V7-V9 would have been abnormal.

So what does this case highlight?

• Approach everything you read with a critical eye, even peer-reviewed journals.
• The 12-lead ECG doesn’t pick up every MI, but with a trained eye you can spot very subtle STEMI’s and greatly increase its sensitivity.
• Have a low threshold for running posterior leads, especially if the patient has ST-segments that are abnormally horizontal or show even slight depression from V2-V4.

The post Seeking the Esoteric, Missing the Apparent appeared first on The Medial Approach to Emergency Medicine.

I’m not that great with mnemonics.

I can never remember all the terms involved, often I screw up the mnemonic itself, and I’m always scared that I’m going to substitute something that isn’t actually part of the differential. It’s as though one day I’m going to debate with myself whether hyperthyroidism falls under “H-for-hyper” or “T-for-thyroid” while reviewing the H’s-and-T’s during a cardiac arrest and miss the patient’s tamponade.

Still, there’s one mnemonic that I live and die by, and that is the DIE acronym for bradycardia.

[D]rugs

[I]schemia

[E]lectrolytes

I stole this differential from the great Mel Herbert and a talk he gives on dysrhythmias. Here’s the bradycardia section of his lecture, posted on the EMRAP-TV website. I initially created this acronym for his differential assuming that it had been documented before, but after a cursory Google search I don’t see anyone else using it, so maybe I’m the first to give it a chance for widespread dissemination. Go-figure.

Now this is far from a comprehensive list of the causes of bradycardia. On the ValueMD site they have an 16-item acronym for the differential of sinus bradycardia alone, which just so happens to spell-out SINUS BRADYCARDIA. Instead, DIE just covers the major reversible players that I am most likely to miss if I don’t force myself to ask, “Could this bradycardia be from drug-effects, ischemia, or an abnormal electrolyte level?”

ECG of a patient with a sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.

I’ve lost count of the number of ECG’s where this simple acronym has saved me from missing the major treatment-changing cause. Usually it’s because I failed to consider effects B-blockers, Ca-channel Blockers, or digoxin. Whether it’s due to an acute overdose, slightly supra-therapeutic levels, or other drug interaction that results in a symptomatic or worrisome bradycardia, all of those causes fall under the heading of “drug-effect.” Still, there’s also a fair share of hyperkalemic and ischemic cases I attempted to overlook as well, so I still walk through all three steps for every patient I see with a slow pulse.

This patient’s K+ was 6.9 mmol/L. Click to enlarge.

In terms of its saves-to-size ratio, this acronym offers the most bang-for-your-buck of any mnemonic I’ve come across. Plus it’s incredibly easy to remember and piece-together.

Enjoy, and let me know how it works for you. I’ve often considered adding hypothermia and changing it to HIDE, but then it loses a lot of the impact factor you get from the word DIE.

edit: Also check out Dr. Ken Grauer’s excellent commentary below. A few minor changes were made to the post as a result, but there’s far more to his insight than the simple rewording I implemented.

The post Don’t Let Your Bradycardic Patient D.I.E. appeared first on The Medial Approach to Emergency Medicine.

People still make Borat references, right?

Anyway, I’ve got a quick one for you today. This patient was being evaluated for possible pericarditis. What’s the rhythm?

Click to enlarge.

Here’s another look at lead II from a different 12-lead. Click to enlarge.

And here’s a third strip of lead II for your consideration. Click to enlarge.

Let’s first discuss what this rhythm is not:

• Sinus arrest or sinus pause (as it was read by one physician)
• Type II AV Block (as diagnosed by another physician and the computer)

So why were these providers mistaken?

• The first was too hasty in his reading. He saw only irregular pauses in the sinus rhythm and wrongfully assumed they were due to inactivity of the SA-node. Looking closely, however, you can appreciate that there is a “blip” in the T-wave preceding each break in the rhythm. This blip is a buried P-wave. Although it’s not followed by a QRS-complex, it resets the SA-node before the next scheduled sinus beat and results in a compensatory pause while the sinus node repolarizes and prepares to resume normal pacemaking.

Red arrows denote buried P-waves. Click to enlarge.

• The second physician managed to avoid that pitfall and picked-up the hidden waves, but then made another common error. If you march out the P-waves in these strips, you’ll notice that the buried ones arrive early in the cardiac cycle and are thus premature atrial complexes (PAC’s). In fact, they arrive so early that the AV-node is still in its absolute refractory period and cannot conduct to depolarize the ventricles. This results in a P-wave that is not technically “blocked,” but instead is what we term “non-conducted.”
  In this case semantics matter. It is the job of the AV-node to keep the ventricles from being overwhelmed if the atria fire too rapidly (i.e. atrial fibrillation), so refusing to conduct these excessively early beats demonstrates that the AV-node is in-fact behaving normally. Saying these P-waves were “blocked” would give the impression that there was pathology involved and carry a much different prognosis.

It’s easy, right? This rhythm is very simply: Normal Sinus Rhythm with Multiple Non-conducted PAC’s.

During your career the number of ECG’s you’ll see with non-conducted PAC’s will far exceed the cases of Type II AV Block. Whenever you encounter a pause in a rhythm strip, remember these two things:

• The most common cause of a pause is a non-conducted PAC,
  and…
• The most common cause of blocked P-waves is not.

The post This Heart is Blocked Not appeared first on The Medial Approach to Emergency Medicine.

We’ve switched from wordpress.com to wordpress.org and now have a new address:

www.medialapproach.com

Setting up redirects and getting the site going under a new host is still very much a work-in-progress, but that’s our new permanent home and where all future posts will show up. Check it out, and make sure you update the links on your fan pages accordingly.

Aortic dissection is a disease that commands a lot of respect. Thankfully, it’s also quite rare, and as a result, we don’t cross its path very often. While the scarcity of this disease is good for the population at large, it ends up being quite detrimental to our individual patients because we simply don’t have a lot of experience identifying it. What follows are just some ideas I’ve picked up over the past few years that I figure are worth sharing and considering…

Why is it so important?

Rare, atypical, and scary: that’s probably the best way to summarize aortic dissection.

Rare – When understanding its incidence, the most usable figure I’ve come across states that it occurs around once per 10,000 patients admitted to the hospital. By my estimate, that means that your average ED with an annual census of 50,000 patients might see one patient per year with this disease. So, if you haven’t seen anyone with a dissection yet, you’re not alone.

Atypical – Of the diseases that can result in your imminent demise, this is probably the most deserving of that title given to so many conditions: “The Great Masquerader.” We all know the classic chief-complaint of “tearing mid-scapular back pain,” but if that’s the only symptom that catches your ear, you’re bound to miss some. It’s been reported that maybe 4.5% of dissection present PAIN FREE, and since the aorta has branches to every part of the body, the constellation of signs and symptoms you encounter can be quite varied.

Scary – Data from the IRAD database suggests an in-hospital mortality of 27.4% for all-comers with a dissection, and that’s without counting all the patients who died prior to arrival or were missed and sent home to perish. A commonly quoted figure is that an acute dissection is associated with a mortality of 1 to 2% per hour for the first 24-48 hours.

The “Dissecting Aortic Aneurysm”

You may disagree, and feel free to state your case, but I absolutely abhor this phrase. When someone uses it, I can’t help but infer that they don’t understand the pathophysiology of either a dissection or an aneurysm. By definition, and common understanding, an aortic aneurysm is a bulging of all three walls of the aorta.

Aortic aneurysm. Click image for source.

On the other hand, a dissection occurs when the intima (inner layer) of the aorta separates from the adventitia (outer layer) by the media (middle) being torn and filled with blood. In the latter condition, the outside dimension of the aorta is likely to change, but all three layers do not do so equally, and thus, it does not meet the definition of a true aneurysm in my book. I hope we can put that behind us.

Aortic dissection. Click image for source.

Not done yet? Well you’re technically right, you can have a baseline aortic aneurysm that eventually leads to a dissection, but such an entity is quite rare – especially considering that plain-ole dissections are rare enough – so I think the term should not be bandied-about unless there is imaging to confirm the diagnosis. In every other case, aortic aneurysm and aortic dissection are two very distinct diseases with differing pathophysiology and management.

The IRAD Database

One of the really interesting things going on in medicine right now is the International Registry of Acute Aortic Dissection (IRAD). You can read more about it here but basically it’s grown to a group of 30 large referral hospitals in 11 countries that are collecting data on pretty much everything you ever wanted to know about aortic dissections. In 2000 they published one of their seminal works in JAMA, covering the initial registry data on 464 patients with aortic dissection. Most of the numbers I quote in this article come from that study unless otherwise noted.

You Can’t Diagnose Every Dissection

As I stated earlier, 4.5% of the patients in the IRAD registry presented with ABSOLUTELY NO PAIN. If you can’t handle the fact that you’re eventually going to miss one of these, you should probably find a different line of work.

“Sudden and Severe”

The classic teaching is that the pain of dissection is described as “tearing,” but that’s only present in 50.6% of cases. In fact, more patients presented with “sharp” pain (64.4%). More useful, instead, is a history of pain that was sudden (84.8%) and severe (90.6%) in origin.

In fact, I actually like to think of aortic dissection as a lot like subarachnoid hemorrhage. They both initiate with sudden and severe pain (maybe maximal at onset?), often with atypical presentations, and both are diagnoses that significantly benefit from early identification and treatment. Also, in my limited experience (maybe two or three cases of each), they are both also very easy to dismiss as “malingering” or “over-dramatic” presentations as a slightly uncooperative patient moves around on the gurney, unable to get comfortable. That is, until you see the CT results and very quickly reverse your opinion.

The “Chest Pain and…” Syndrome

As mentioned in the title, one of the most important points of this discussion is that you should consider the diagnosis of dissection in any patient complaining of chest (72.7%) and/or back (53.2) pain AND something else. What can that something else be?

Abdominal pain (29.6% reported any) – also a possibility on its own.

Arm or leg pain.

Focal neurological findings – any stroke-like presentations (4.7% presented as cerebrovascular accidents), including arm, leg, or facial paresthesia, weakness, or paralysis.

Syncope (9.4%).

Altered mental status.

Or pretty much anything else that strikes you as weird and not typically related to the chest and back pain we encounter.

Why This Myriad of Presentations?

Consider for a moment what this giant artery connects to: everything! If you tear apart the layers of your aorta, you can also block blood-flow through any of the arteries coming from it.

Aorta and major arteries. Click image for source.

Disrupt flow through a renal artery, and that kidney is going to die.

Dissect into an iliac and the patient may experience leg pain, weakness, or hypo-perfusion.

Same goes for the bracheocephalic or left subclavian arteries, affecting the arms.

Hit those same arteries, and it can in-turn block a carotid, causing the patient to present like a stroke.

Cut off flow to part of the spinal cord, and you’re going to see weakness, paresthesia, or paralysis affecting the downstream extremities.

Hit a mesenteric (gut) artery, and the patient will experience severe, unremitting abdominal pain, and eventually dead bowel.

Dissect back into the pericardium, and it’s going to fill with blood and lead to tamponade, with signs of obstructive shock.

Here’s a SCARY – but rare – one: hit a coronary artery, usually the RCA, and you’re going to see a STEMI on the ECG (3.2%). So, in that case, you’ll have a patient who presents with chest pain and an acute MI, maybe even in CHF (6.6%), but their underlying problem is actually an aortic dissection. Give them heparin or lytics and that’s what Dr. Amal Mattu likes to call a “clean kill.” I like to call it an impossible diagnosis.

So How Do You Die from Dissection?

The quickest way is through aortic rupture, which carries a 50% prehospital and 80% overall mortality.

As mentioned earlier, you can also dissect back into the pericardium, fill it with blood, and die from tamponade.

Or, from that last scenario, there’s also a small chance you can block one or more coronary arteries, and perish from a heart attack and sudden cardiac arrest.

Severe aortic insufficiency from poor flow through the aorta, along with an incompetent aortic valve, can also lead to poor perfusion and death.

Then there’s slower routes, like infarcting a kidney, some gut, or your brain, and passing away from the sequelae that those conditions bring.

How Does Blood Pressure Fit Into the Patient Assessment?

Chronic hypertension is a well-known risk factor for developing a dissection, but what does it mean if the patient in front of you is hyper- or normo-tensive?

Almost nothing. 49% had a systolic BP >149 mmHg (hypertensive), and 34.6% had a BP from 100-149 mmHg (normotensive), so the patient’s current BP doesn’t do much to help you out. Unless, that is, it’s low, in which case you’ll hopefully be able to recognize that something catastrophic is happening.

What is the Role of Bilateral Blood-Pressure Measurement?

Here’s one of my favorite topics…

When I first heard of doing bilateral blood pressures to look for pseudohypotension in ascending aortic dissection, I thought it was the greatest idea ever. If the patient managed to kink off one of the arteries going to an arm, it would result in a false-low blood-pressure reading. As a result, I did a lot of bilateral pressures, got a lot of false-positives, and didn’t save anyone.

One problem arises when trying to decide just what constitutes an abnormal difference, with various sources quoting 10, 15, 20, or 30 mmHg as worrisome levels. I’d say 20 mmHg is the most common value cited, but that raises another issue.

Maybe 19% of the general population also has a 20 mmHg difference between their arms at baseline. It gets worse when you consider that the greater a patient’s atherosclerotic burden, age, or hypertension – three of the big risk factors on our radar – the more difference you’re going to see between their limbs. Then there’s the additional variance involved in performing the same test twice, which will result in slightly different results every time. PLUS, what if the dissection is affecting both arms, and as a result, both blood pressures are diminished, but at equal levels.

So, What’s the Alternative?

The basic physical exam: pulses and perfusion. Simply check pulses in all four extremities, ensure that  there are signs of good perfusion, and both you and the patient are in good shape from that perspective. You haven’t ruled out a dissection by any stretch, but a positive result would greatly increase the chances that there is actually a dissection. With bilateral BP’s, on the other hand, you still cannot come close to ruling out dissection, but a positive result is also a lot less useful.I don’t have exact numbers, but if you know how to think in likelihood-ratios, pulse deficits would have a much higher positive-LR than bilateral BP’s (just throwing out an example, 15 vs. 4), but both would have similarly useless negative-LR’s (again, made-up, 0.7 vs. 0.5)

Radial and femoral arteries are my sites of choice.

Radial pulses are usually readily palpable and can be compared simultaneously, so I like to start there. The lower extremities are less straight-forward, but I find the femorals are simple enough to find on most patients, easy to compare consecutively, and only inches away from the lower quadrants of your abdominal exam if you’re doing it right. On the other hand, if you try using pedal pulses, you’re likely to get a lot of false-positives when the patient simply has difficult anatomy. Still, even when using the femorals, it’s worth looking at their feet to get a feel for both symmetric and overall perfusion.

In Conclusion…

This disease is scary, rare, tough to diagnose, and easy to mimic. I guarantee that on your next shift you’re going to see at least one patient who now raises some flags on your dissection radar. Thankfully, that’s the point! It’s worth having a high suspicion for this disease.

With that said, please don’t go chasing zebras. I don’t advocate treating the patient with an exacerbation of their chronic back-pain and sciatica like they’re dissecting (but they still can…). Instead, use that encounter as an opportunity to open your differential a little and practice performing a slightly more thorough history and physical exam. The goal isn’t to rule out the disease in everyone with back pain, but rather to risk-stratify them as “not going to die in front of me.”

If you have any more pointers, or disagree with any of my opinions, let me know! As always, I’m open to discussion – yes, even with you, guy who still calls it a dissecting aneurysm.

Testing for arm drift is a standard part of the simplified three-part neurological exam we all perform, technically called the Cincinnati Prehospital Stroke Scale. It’s a fairly crude examination, but when even one finding is positive in the right clinical scenario, there’s a pretty good likelihood that the patient has experienced a stroke. The problem is that testing for arm drift isn’t perfectly sensitive and it will miss a certain number of acute lesions that could be amenable to treatment.

One way to increase the yield of the physical exam is to expand beyond the basic maneuvers we are taught early in training. Doing so, however, has costs in terms of time and memory, two things we are often short of in emergency medicine. We can’t afford to be doing complete neurological exams, nor remember the numerous steps involved, but by adding a couple of simple, high-yield maneuvers to our repertoire we can really improve our patient assessment.

Arm Drift in Summary

First, let’s review what we’re already doing. The finding we really want to elicit with arm drift testing is actually called pronator drift, which has a bit more to it than just looking for unilateral arm drop. Like we all know, you start by having the patient hold their arms straight out in front of them at the level of the shoulders for 10 seconds (or 20, or 30, depending on who you ask). The trick most people know but don’t always utilize is that the patient’s eyes should be closed and their palms pointing towards the ceiling. If you’re not doing these last two parts, you’re giving up valuable information. A positive test will usually exhibit an inward rotation of the patient’s affected hand (pronation), plus-or-minus downward arm movement. In certain cases, however, you may actually see the affected arm move upwards; just know that a normal person should be able to keep both hands parallel. I also like to tap their hands downward after several seconds to look like I’m doing a deluxe exam and see if I can provoke any subtle weakness.

The Alternative

So onto our new concept: the “forearm rolling test.” Unlike most signs in medicine,  I don’t believe this one has a fancy eponymous name meant to confuse medical students. To perform the exam, you have the patient hold their arms in front of them with their elbows bent at 90 degrees and forearms parallel to the ground. The patient rotates their arms around one-another in a circular motion for 5-10 seconds, then reverses direction. A positive test will result in the affected arm remaining fairly stationary while the good arm circles it. Pretty straightforward.

Forearm rolling test. Click image for source.

So below is the only video I could find on the internet demonstrating the maneuver. For best results, I suggest having your partner play a hand drum while you perform the exam. Glittery belts are strictly off-limits unless you are an attending neurologist.

Forearm Rolling (sorry I couldn’t get embedding to work)

The Evidence

I first came across this exam in a wonderful book called Evidence-Based Physical Diagnosis. For the forearm rolling test they listed a sensitivity of 87%, specificity of 98%, positive LR of 36.6, and a negative LR of 0.1 in identifying unilateral cerebral hemispheric disease. There’s not any discussion of the numbers outside of the table where they are listed, but they seem to come from a study by Sawyer et al in 1993.

Even without a full-text article available, it’s obvious that these numbers are too good to be applicable to a population outside of the very specific one studied. Still, the results certainly caught my attention and made a case for the arm roll being a potential useful tool. Reviewing a couple of textbooks and the abstracts from 3 or 4 other studies, the sensitivity of the test ranges anywhere from 24% to 98% depending on the population being studied. The important point is that it consistently outperformed pronator drift in the detection of cerebral lesions. It’s not perfect, but it’s probably an improvement.

There are two variations on the maneuver that I’ve come across in the literature, referred to as index-finger rolling and thumb rolling. The problem is that while they are mentioned fairly often, they are not well described and I don’t have access to any of the articles that might provide some elucidation. Why should you care about these? Well it appears that finger rolling may be even more sensitive for cerebral lesions than forearm rolling, with thumb rolling claiming an even higher sensitivity than both.

As a point of disclosure, I just came across these variations while researching this post and haven’t used either in clinical practice, but I will be certainly trying them in the near future.

Finger Rolling

CONJECTURE ALERT: My only source of information on how to perform this test comes from this one picture I stumbled across. It looks like it’s performed very similar to forearm rolling, but with the index fingers extended and the focus on rotating the hands as opposed to the entire arm.

Finger rolling. Click image for source.

Since most sources mention this as being superior to forearm rolling, I’m not sure why they even bother mentioning the latter anymore. Still, there’s not too much hard data out there so try out both and see what you like best. Here’s the one free full-text article I could find comparing the two, and a letter describing why it’s plausible that they could be useful in combination.

Thumb Rolling

DOUBLE CONJECTURE ALERT: I don’t even have a picture of this one to go off, but I’m going to assume that thumb rolling as described in the neurology literature is basically the act of twiddling one’s thumbs. Amazingly enough, someone put a video of himself twiddling his thumbs on YouTube, so here’s the enthralling link if you’re not sure what I’m talking about.

There’s only one abstract I was able to find on the subject. The premise is that since finger rolling is better than forearm rolling, examining the even more distal thumbs will provide greater sensitivity as they are more likely to be affected by a CNS lesion. Again, this is pretty limited data and all I can suggest at this point is that you try it out and see if you like it.

Conclusion

So how do I plan on using these tests? Since drift is a standard part of the Cincinnati Prehospital Stroke Scale and commonly understood by emergency care providers of all levels, I don’t see it being replaced by rolling. Using the two in tandem certainly seems like a good idea to me, with almost no downsides. All of the rolling tests are so quick and easy to perform that the only negative would be the risk of a false-positive result.

In my limited experience the false-positive rate is small, easily predicted, and no worse than what you see in pronator drift testing. In fact, I find the forearm roll is actually a bit easier for the patients to perform than pronator drift testing. We see a lot of folks who are either too weak and lethargic to hold both arms up for a decent amount of time, or don’t follow directions very well and get distracted after a couple of seconds, so 5-10 seconds of active participation by having them roll their arms usually works pretty well.

Finger rolling will probably be my new default maneuver over forearm rolling. The consensus in journal articles and neurology texts seems to be that it is more sensitive, plus I imagine that it also is a bit easier for the patient to perform. I’ll still have to try them out in tandem for a bit to make sure this pans out, but I don’t foresee any issues.

As for thumb rolling, I’m much less sure how this is going to fit in at this point. For now it will just be something I play around with when I have the opportunity. If I decide I like it, I’ll update this page to reflect my experience.

So get out there, do some exams, and let me know what you think.