Is the shoulder in? Use ultrasound!

It was a classic “good news/bad news” sign out.

The  attending who was signing out to me admitted that this wasn't the cleanest sign-out, but they had a plan.


The bad news: the patient likely had a shoulder dislocation, but the read on the X-ray was equivocal.

  

"Can I order a clinical correlation?"

Given this unclear picture, the plan was to try sedation, and pop it back in place. 

The good news: the attending had already tasked a senior resident and the orthopedics PA-C to perform the sedation and (attempted) reduction, and they were champing at the bit to do the procedure. 

My evaluation

I looked at the X-ray, and re-examined the patient. As he was young chubby guy, it was difficult to be sure of the exam. Since both my exam and the X-ray were so unhelpful, I stalled the resident and PA-C while I grabbed the ultrasound.

Now, ultrasound is not usually thought of as a great test for shoulder dislocation. The usual approach to definitively excluding a glenphumeral dislocation (especially posterior dislocation!) is to obtain an axillary view, shooting up through the armpit. And of course we can always get a CT of the joint.

But you can get much the same image with the ultrasound. So, placing the probe on the posterior shoulder, I aimed anteriorly, with the left side of the screen oriented to the lateral aspect, like this:

This produced a clear image of the glenohumeral joint:

 

As usual, US is best appreciated dynamically, with this clip showing the patient rotating his arm:

I hope you can see how the head of the humerus is well-seated in the glenoid. But despite this dazzling proof, x-rays and a CT were needed to convince ortho that the shoulder was not dislocated, and that no sedation and tugging were needed.

The (ionizing radiation) proof

The axillary view of the shoulder X-ray (needs to be specifically ordered), oriented similarly to the US:

 The CT of the shoulder, with the slices and orientation similar to the US:

If you want to check out some other US examples of dislocated shoulders, you can also check out this great video from ALiEM:

Ultrasound for the ... Wait, what?!

I would have liked to say this was an ultrasound win, but I'm not so sure. The downsides of this approach, in retrospect, were:

• The patient didn't get to enjoy some of our high-grade ketamine;
• We didn't get to high-five each other after our "subtle reduction;" and
• The resident was cheated out of a procedure!

So, know the downsides ahead of time.

High-flow nasal cannulas: Not yet ready for ED use.

What is high-flow nasal cannula (HFNC) therapy, and, more importantly, does it work? A recent segment on EM:RAP went into a fair amount of detail about the putative mechanism, so I’ll leave that alone.

What that segment left out, though, was any discussion of the published evidence pointing to the benefit of HFNC. And indeed, while there are a lot of anecdotal reports and personal testimonials, the actual data hasn’t been clearly discussed. Here’s a quick review of what we currently know.

1. Preterm infants

Although the “diet-PEEP” argument would suggest that HFNC might have a large role in tiny patients, it isn’t clear that HFNC helps prevent intubation in preemies. A Cochrane review suggested that using HFNC post-extubation, instead of CPAP, might lead to higher re-intubation rates. An RCT that was conducted after that review, however, found that HFNC was roughly equivalent to nasal CPAP for respiratory support in this age group. Data from other recent trials haven’t been as convincing, though, and many neonatologists still find the evidence “insufficient” to use HFNC in place of more established therapies

2. Infants

It may help prevent intubation of little kids with bronchiolitis, although the data is weak. The two most relevant studies were retrospective chart reviews, using a before-and-after design, looking at overall rates for intubation in the time period after HFNC was introduced to the pediatric service. Nonetheless, McKiernan found that intubation rates for bronchiolitis dropped from 23 % to 9%, and Schibler found the rate plummeted for 37% to 7%!

McKiernan 2010

This may end up being one of the best-supported roles for HFNC, and high-quality studies are in progress that could help clarify the issue.

3. Adults

The initial trials in adults have demonstrated modest improvements in oxygenation, but haven't studied patient oriented-outcomes. For example, one study found that oxygenation mildly increased after HFNC initiation, but no control group was used.

Sztrymf 2012

In one controlled trial, versus face mask, fewer desaturations were seen with HFNC. Despite this, there was no statistical difference in the use of rescue CPAP/BiPAP. A few other studies have further noted that HFNC seems to be more comfortable than CPAP.

A single-author review, otherwise very bullish on HFNC therapy, conceded: “although some clinicians may have the impression that in some instances, use of HFNC has avoided intubation, this has not been shown in a controlled trial.”

The largest current review on the use of HFNC concludes that (my emphasis):

“While theoretical advantages exist over standard nasal cannula and face mask oxygen, current evidence does not definitively demonstrate superiority to other methods of respiratory support. Few studies have focused on clinical outcomes beyond common respiratory parameters. Given the potential lack of consistency of positive pressure generated with current HFNC systems, NIV such as CPAP and bilevel positive airway pressure should still be considered first line therapy in moderately distressed patients in whom supplementation oxygen is insufficient and when a consistent positive pressure is indicated.”

Bringing it home!

Being an “early-adopter” is cool – if you’re lining up to get the new iPhone or Zune! In medicine, however, it doesn’t often pay to jump on a bandwagon before the data is in. (Want to buy some Xigris cheap?) We are being encouraged to try a new therapy that uses proprietary (proprietary = $) devices, with soft indications, scant evidence, but with touted outcomes such as “improved comfort,” instead of mortality or rates of intubation. We should be cautious.

Particularly concerning is the uncritical enthusiasm for the use of this device in situations that either clearly call for other therapies, or for no therapy. For example, some describe the utility of HFNC in patients who are “extremely hypoxic,” but there is little evidence that HFNC improves outcomes in this population.

HFNC is probably more useful for precisely titrating FIO2 in the (mythical?) CO2 retainer. But if there is a concern about the PaCO2, why not use a proven therapy like NPPV that we know saves lives?

Lastly, some clinicians promote the use of HFNC for CHF, since there is (wink, wink) a “PEEP component,” but that’s a patient who needs CPAP or BiPAP as well, since we already have proven a mortality benefit in that population as well.

Sure, you can relax, talk with family, and eat while wearing HFNC, but if you are so dead set on wolfing down a sandwich, you probably don’t need an expensive, unproven therapy. You need 2 liters per minute, and a floor bed!

Femoral pulse during CPR - Arterial or Venous?

There are many uncertainties about how each of us will die.

Based on my experience in the ED, however, many of us will spend our last minutes on Earth with a stranger's hand shoved into our groin.

Your own hand? Fine.

I'm talking about the checking the femoral pulse during CPR, of course. It's a well-enshrined part of our resuscitation practices, but what it is it actually telling us?

The Theory
The idea, of course, is that effective CPR will produce an arterial pulse, albeit weak, that will generate a cardiac output about 20% of normal. Palpating a femoral pulse during compressions supposedly verifies that the CPR is being effectively delivered.

Evidence that the femoral pulse is venousHowever, there is some uncertainty about what a palpable femoral pulse actually represents. Hilty used ultrasound in a study of central line placement during cardiac arrest, and noted that 9/20 patients appeared to have femoral venous pulsations, rather than arterial.

Note that this was in the dark ages of ED ultrasound (1997), back before Christian Doppler was born. 

Based on this finding, as well as on a case report of two kids getting open-chest cardiac compressions, many people now believe that the femoral pulse during CPR is just the venous back-flow. A video posted by an emergency physician in Qatar supports this view, where he demonstrates interrogation of the femoral vessels with power doppler during CPR:

The femoral vein shows much brighter signal than the artery, suggesting that the venous flow far exceed the arterial. Of course, since this is power doppler, we don't know the direction of the flow.

Evidence that the femoral pulse is arterial?
Cardiac arrest, asystole when EMS arrived in the ED, the LUCAS dutifully chugging along.  

Probe placed in the right groin, angled cephalad slightly. First, with color doppler:

The femoral artery seems to show a fairly well-defined arterial pulse, while the femoral vein has a turbulent, almost "yin-yang-like" character, that does not suggest effective flow. So based on this clip, it seems like the femoral pulse indeed reflects arterial impulses, not venous.

(BTW, here's a clip of the same view, while the LUCAS was taking a break. Just so you know that there was no spontaneous cardiac activity mucking up the doppler.)

So, what does the femoral pulse tell us about CPR quality?
Not much, probably. The scanty and conflicting "evidence" (i.e. collection of anecdotes) reviewed here doesn't make it clear if pulsations in the groin are coming from the artery, the vein, or perhaps even both. This looks like a promising avenue for an emergency ultrasound study!

In the meantime, assessing the quality of CPR is likely best done with end-tidal CO2, although a recent Ultrasound Podcast episode suggested using focused echo  to optimize compressions. 

Septic hip in Kids, part 2: This time it's personal...

I wrote about the "textbook" approach to differentiating the septic hip from plain ol' synovitis in a previous post Septic hip in kids: 5 myths of ED evaluation. Today, I want to review a real case of mine, and highlight both the weakness of the older methods, and the advantages of the newer perspective.

The Case

A 4 year-old male complained of pain in his hip, bad enough that he couldn't put his weight on it. It had started 1 day ago, but had worsened despite acetaminophen. There was no significant recent trauma. He has seemed ill yesterday, though, and while the parents had not taken a temperature, he had "felt hot," and had some mild chills. His temperature in the ED was 100.2.

His right hip was held in slight flexion and external rotation, and he could not bear weight. Labs were obtained, and showed a WBC of 12.2, and (after hours of waiting) and ESR of 28. The CRP doesn't get run at night.

Were the Kocher criteria helpful? (Spoiler: No!)

Kocher-type criteria are applied to help decide on the need to perform an ultrasound, and then decide on the need for aspirating a hip effusion if it is found on US. How did our patient do?

• Non-weight-bearing - 1 point
• Temp < 38.5 - 0 points
• WBC > 12 - 1 point
• ESR < 40 - 0 point
• CRP - not available

So, 2 points, which means that he has a probability of having septic arthritis of...

Sultan 2010

... somewhere around 11 - 60%. But notice that if the WBC had been just trivially lower, say 11.8 instead of 12.2, we would have only had 1 point, and the risk would have dropped to 3- 36%.

Heck, say we also had given him a strong analgesic, and he was then able to walk a little. He would have then had 0 predictors, and so only had a risk of somewhere between < 0.2% and ... 17%???

Clearly, these criteria are not helpful at "ruling-out" the possibility of septic arthritis, so I decided to decide by looking at the hip.

Was Ultrasound helpful? (Spoiler: Yes!)

Quick guide to placing the probe :

From Tsung and Blaivas

First I checked the "good" hip, the left side:

I then checked the "bad" hip, the right:

Looked like there was a difference!

Generally, any effusion greater than 5 mm, or 2 mm greater than the contralateral side, is considered positive. This looks pretty unambiguous, and the radiologogist agreed, and told me that a formal ultrasound was not needed in this case.

Clinical course:

The hip was aspirated by IR in the ED (Those guys are total champs at this, but I'm doing this next time! Very straight-forward.), and the patient admitted. The cell count cam back quite high, around 100,000 white cells/ml, which would have placed this patient as a "true positive" case of septic arthritis in almost any study.

However, by the time this result came back, the patient was tearing around the pediatric floor, completely asymptomatic. The culture never grew out an organism, and he was discharged as a transient synovitis.

Bottom Line:

This was the first time I had a patient where I was truly concerned about septic arthritis of a pediatric hip. The use of US clarified the diagnosis early in the visit, and pointed to a greater role in future case. As I highlighted in my prior post, use of point-of-care US in the ED has the potential to "flip" the older diagnostic and therapeutic pathway - use it!

Pulmonary Embolus: See the echo, and believe the ECG!

Too many people are nihilistic about studying the ECG for signs of PE, and believe that the ECG is too non-specific to play a role. In particular, two beliefs stick in my craw:

“The most common sign of PE on the ECG is tachycardia”

This is not necessarily true. For example, Ferrari found that TWI in V1-V4 was far more common in PE (68% of patients) than was sinus tachycardia (only 36%). Likewise, the average heart rate in Kosuge’s 2007 study was only 94!

“PE = S1Q3T3”

S1Q3T3 can be very specific for PE, and is helpful to note. But it isn’t the only thing to look for on the ECG, and the poor sensitivity of this sign could mean missing a PE. Kosuge has found that only 20-22% of PE patients had an S1Q3T3, while the TWI in leads III and V1 was far more sensitive.

The Case

An 80-something year old male was brought to the ED by EMS, feeling weak. 

He said that this had been going on for about a week, and was getting worse. Only when directly queried did he admit to orthostasis, and in fact had syncoped while shopping the day prior. He denied any chest pain, but endorsed some mild dyspnea.

He had a history of CAD, PCI, and a remote history of a PE. His memory and the records were vague on this last point, and he was not on anticoagulation.

His vitals and exam were unremarkable. Since this could have been ACS, or even mild CHF, a troponin and BNP were ordered.

The ECGs

An ECG was immediately obtained:

The baseline wanders, but there is a clear S1Q3T3. Furthermore, there is T wave
inversion (TWI) in the anterior leads, from V1 to V5,. These findings suggest RV strain

Kosuge showed in 2007 that, in patients with anterior TWI and symptoms suggestive of either ACS or PE, TWI in both leads III and V1 strongly favored PE over ACS.¹ 

A recent update from Kosuge confirms and extends those results, demonstrating that TWI in both leads III and V1 and/or peak TWI in leads V1 or V2 was extremely sensitive and specific for PE (versus ACS due to LAD occlusion).²

So, the ECG proves it, right? Unfortunately, when the emergencu physician reviewed the ECG from 5 months prior...

An arguable S1Q3T3, and TWI in III and V1-V4.

… and from 7 years prior...

'Bout the same.

... it seemed like the ECG findings were, perhaps, simply chronic. Well, when in doubt, break out the ultrasound!

The Echos

Parasternal long-axis

There is a dilated and hypokinetic RV, while the anterior wall contracts nicely.

Parasternal short axis

Septal bowing, or D-shaped septum (“Movahed’s sign?”)

Apical 4-chamber

Markedly dilated, hypokinetic RV free wall, with preserved apical contractility
(a.k.a. McConnell’s sign)

Triscuspid valve – color Doppler

Moderate regurgitation,  max velocity 5 m/s by CW Doppler, indicating very high pulmonary artery pressure

Clinical course

Given the patient’s CKD, and the stable hemodynamic status, unfractionated heparin was started, and the patient was admitted. A V/Q scan the following day confirmed an acute PE, apparently with significant chronic emboli as well! Anticoagulation was bridged to oral therapy, and the patient was discharged back home.

Bottom line:

The ECG can be very helpful is suggesting PE. Many physicians are nihilistic about studying the ECG for signs of PE, and believe that the ECG is too non-specific to play a role. 

In particular, two elements of the conventional wisdom are often uttered without considering the evidence:

“The most common sign of PE on the ECG is tachycardia”

This is not necessarily true. For example, Ferrari found that TWI in V1-V4 was far more common in PE (68% of patients) than was sinus tachycardia (only 36%).³ Likewise, the average heart rate in Kosuge’s study was only 94!

“No S1Q3T3 = no signs of PE”

S1Q3T3 can be very specific for PE, and is helpful to note. But it isn’t the only thing to look for on the ECG, and the poor sensitivity of this sign could mean missing a PE. Kosuge found that only 20-22% of PE patients had a PE,¹,² while the TWI in leads III and V1 was far more sensitive.

Perhaps the ECG isn’t completely sensitive for picking up every tiny sub-segmental embol-ette.  Remember, though, that the ECG isn’t that sensitive for picking up every little troponin leak either! But the ECG is darn good for picking up the STEMI patient that needs emergent therapy, and the analogy with PE is likely true as well – the ECG will suggest the diagnosis in patients who are at high risk from large PEs.

1.         Kosuge M, Kimura K, Ishikawa T, et al. Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves. Am J Cardiol. 2007;99(6):817-821. doi:10.1016/j.amjcard.2006.10.043.

2.         Kosuge M, Ebina T, Hibi K, et al. Differences in negative T waves between acute pulmonary embolism and acute coronary syndrome. Circ J Off J Jpn Circ Soc. 2014;78(2):483-489.

3.         Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M. The ecg in pulmonary embolism : Predictive value of negative t waves in precordial leads—80 case reports. Chest. 1997;111(3):537-543. doi:10.1378/chest.111.3.537.

Septic hip in kids: 5 myths of ED evaluation

I had 5 year-old brought into the ED last week, not able to walk on his right leg, or even to move his right hip around much at all. The day before, he had been hopping around to avoid using the leg, but on the day of the ED visit it hurt too much to even do that. Like any active boy, he had had a few recent tumbles, but nothing that he didn't stand up right after. His mother said that he had felt warm at home, and she suspected a fever.
Of course, I was thinking "This either septic arthritis (SA) or transient synovitis (TS) ... how does this again?" So I turned to some trusted EM references, and was reminded of the

THE FOUR BIG RULES

1. The WBC, ESR, and temp can rule out septic arthritis.
2. Send the kid to radiology to get an US of the hip.
3. Send the kid to IR to get the effusion drained.
4. Consult ortho early for help.

At the end of the night, we did the right tests, found some answers, and treated the patient. But looking over the literature the next day, I decided that I would do things differently the next time. Why? Because those FOUR BIG RULES all had problems, and seem especially outdated in this era of emergency physician-performed ultrasound. The RULES aren't really myths, but they are at least only "quasi-truths."

Let's tackle each of them.

"The WBC, ESR, and temp can r/o septic arthritis."
A predictive tool, using the WBC, temperature, ESR, and the ability of the child to walk, was developed back in 1999 by Kocher. While that initial study suggested that using these factors had the potential to rule out SA, a validation study did not show the same utility. Even a new, prospective algorithm, that added a CRP shows limitations, allowing up to a 6% false-negative rate in non-weight-bearing kids.

Part of the problem with these studies is that most of them are retrospective, and/or enrolled very high-risk patients. For example, 1 out of 3 patients in Kocher's validation study had septic arthritis, a very high proportion, while Caird had an even higher rate of SA! On the other hand, Singhal had far more cases of plain ol' TS.

From Singhal

Why does this matter? Because with these radically different populations, it's real hard to derive and validate a decision rule that works in our typical ED patient. Even if you have a kid who can walk, has no fever, and has a normal WBC, ESR, and even a normal CRP...

From Sultan

... you still have a risk of septic arthritis that is somewhere between 0.2% and 17%!

So, if you are going to rely on the labs, temp, and physical exam to avoid doing imaging and arthrocentesis, you have to be willing to ask right now:  

What percent of cases of septic arthritis are you willing to miss? 

I'm betting that your number is closer to 0% than 17%, so you probably should get some imaging!

Speaking of which...

"Send the kid to radiology to get an US of the hip."
Emergency physicians can reliably us ultrasound to find fluid collections in the pericardium, the lungs, and even in the belly. As for joints, we're used to looking for effusions in the elbow, shoulder, knees and ankles. Heck, it doesn't seem like there's a body part that we don't scan for an effusion.

Why should the hip be different? Should we routinely outsource this to radiology, or can we take care of this?

We can probably handle most of these on our own, without having to undergo intensive or prolonged training. As it turns out, even ED physicians with very limited US skills can be quickly trained to be quite accurate with finding hip effusions. 

In a study conducted in a pediatric ED, physicians with only "minimal" prior experience with ultrasound were trained to find effusions in the hip. The training consisted of a 30-minute teaching session, along with 10 practice scans. They only had to find one "positive" scan before being considered adequately trained for the study. How did they do with this crash course - what was their accuracy?

Pretty good!

Of course, if you have a questionable US finding, or you get a result that is discordant with your clinical sense, you should get confirmatory imaging from our friends in radiology, just like we do in other cases!

"Send the kid to IR to get the effusion drained"
Whether it's an abscess, an effusion, a vein, an artery, peritoneal or thoracic fluid, emergency physicians have gotten pretty good at sticking needles into hypoechoic things. So we can probably handle sticking needles into a clear hip effusion!

The literature bears this out. For example, back before he was blogging about ECGs, Stephen Smith reported on a hip he drained back in 1999! Pretty OG... Since then, EPs at NYU and at Boston Medical Center have reported on their experience on draining these themselves (SPOILER: their experiences were good). 

For techniques and tips, I'll refer you to those papers above, as well as an excellent podcast - Check out the Ultrasound Podcast - episode 38, with Mark Goodman.
"Consult ortho early for help."
Just as for every other patient in the ED, we are the folks who are ultimately on the hook for evaluation and management.It's our responsibility if:

• Ortho says "His CRP is low - you don't need to tap the hip."
• Radiology says "We can't US that now - just keep them in the ED until 8 am." 
• IR says "Why don't you just admit them, and we'll tap sometime tomorrow. Also, hold on antibiotics until we get a sample."
• Anesthesia says "We're not going to sedate the kid in the IR suite at this hour - why don't you do it!"

In the end, it's our patient up until admission or operation.

The Bottom Line
It looks like, as we get better at US and diagnosis, we're creating more work for ourselves. Good!

Women, ACS, and "atypical" symptoms - new study

I was excited to read the new study "Sex-Specific Chest Pain Characteristics in the Early Diagnosis of Acute Myocardial Infarction." My excitement was tempered when I saw Ryan Radecki's take on the article, however.  

"Fundamentally flawed" - ouch.

True, the study by Gimenez et al. cannot prove, because of study design, that men and women have similar rates of atypical symptoms of ACS. However, I’m not sure that this makes the study fundamentally flawed, let alone “comical.” It’s too easy to criticize a study for not being a highly-powered, well-controlled (yet externally valid!) “gold-standard” investigation. But how do we proceed until that rare trial is conducted? In the meantime, why not analyze this study on its own terms? 

Most importantly, this was a prospective study of undifferentiated chest symptoms. Too much of the literature that is cited on this topic uses registry data, or only enrolls patients with confirmed ACS, or interviews subjects long after the onset of symptoms. While the study by Gimenez et al. may not be perfect, its methods are far more robust than most other literature in this area. Importantly, the results triangulate well with other kinds of evidence out there.

1. In most diseases, women have the same symptoms as men. 

How many other diseases are said to show a gender-based difference in presentation? Not many, it seems - I’m pressed to come up with another example where the literature even suggests a significantly different symptom complex.

Indeed, many studies point to the absence of differences in various condition. For example, men and women with pulmonary embolism seem to have similar rates of various symptoms. Interesting, since PE often produces the same sort of vague, poorly localized symptoms as ACS. Along the same vein, at least one study suggests that pancreatitis presents much the same in women as in men. 

Well, instead of symptom differences in heart attacks, how about “brain attacks?” Again, it seems that there are few clinically significant differences in the way men and women describe their stroke symptoms.

Even in appendicitis, a condition that manifests in protean ways, and involves anatomy that sits right next to gender-defining organs in the pelvis, it seems that women have pretty much the same symptoms as men!

So, if there are few (no?) other conditions in which men and women are understood to have clinically significant discrepancies in their symptoms, why should we believe that heart disease should be the rare (sole?) exception?

2. Evidence from the cath lab suggest men and women have similar symptoms. 

Balloon occlusion during PCI is, essentially, a temporary MI. The lumen is occluded for however long it takes to open the artery and deploy the stent, and people can have significant ischemic symptoms during this period. This makes for a great study setting - although we aren’t studying symptoms associated with ACS sensu strictu, we are able to prospectively survey the patients about their symptoms not only after artery occlusion, but before and during as well.

A team in Japan did just that, and found that men and women had chest pain-free occlusions at about the same rate, 35%. Another study, in Canada, also found no difference between men and women in the cath lab.

3. Many studies in this area are not designed to address the crucial question. 

Most of the data looking at men’s and women’s symptoms in ACS come from studies that enrolled patients with confirmed ACS. For example, in the Gimenez et al study, they cite a number of studies that suggest that women present with atypical symptoms more often. Unfortunately, Goldberg 1998, Goldberg 2000, and Dey 2009 all examined only patients with diagnosed ACS. As such, they can answer the question “In patients with an existing diagnosis of ACS, do women and men have different symptoms?” They cannot speak to how to approach the patient with undifferentiated chest pain. 

For example, many of these retrospective studies find that women describe back pain somewhat more often than men. But, what if women without ACS also describe back pain more often than men? If this were the case, back pain would not really be useful as an “atypical” symptom. 

It's worth pointing out that one of the few prospective studies, looking specifically for atypical symptoms in men and women, found that women presented typically more often than men!

Wrapping up...

So, while this study may not be the last word on the subject, it provides yet another high-quality element of evidence pointing towards the same conclusion: Both men and women - old and young, diabetic and not - can have typical or atypical symptoms of ACS.