Monday, December 15, 2014

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:

video

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

video

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!




Saturday, December 13, 2014

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
video

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

Parasternal short axis
video

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

Apical 4-chamber
video

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

Triscuspid valve – color Doppler
video

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.

Wednesday, July 16, 2014

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!


Monday, December 2, 2013

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.

Sunday, July 21, 2013

Lime's Disease - some underappreciated elements.

This is not meant to be a comprehensive review of B. burgdorferi, the life cycle of I. scapularis, or all the other stuff that belong in a thorough introduction to Lime's disease. Instead, I just want to highlight a few aspects that seem to have been under-appreciated.

First, an exacting review of the anatomy of I. scapularis...

This depiction is actually more realistic than how some CT politicians view ticks and Lyme disease.

#1 The "bulls-eye" rash, while classic, is uncommon.
Anytime a sign is described as classic, you ought to expect that,
basically, you will never see it. My rule of thumb when being pimped about how often you see a "classic sign" is to reply "Well, recent research, ah, I believe, shows a lower rate in the modern era, ah, about 15% I believe."

And the literature on erythema migrans (EM) backs me up. A "bulls-eye" pattern, with central-clearing, may have been more common years ago, when Lyme took weeks to diagnose. In contrast, a study from 2002 found that only 9% of confirmed EM had central clearing. Instead, the majority either were homogenous, or were darker centrally!



In fact, central clearing occurred at the same rate as rashes which had vesicles or a blue center.

So, all these are erythema migrans:
Central vesicles (source)
Central raised punctum (source)
Triangular, rather than round (source)

What should you look for, if not a bull's eye? Five key elements are:

  • Blanchable erythema,
  • Flat, with non-raised border. 
  • Large, and rapidly expanding (20 cm2/day).

#2 Don't routinely get "Lyme tests."
The patient lives in suburban Connecticut, it's July, they describe "flu-like" aching and chills, and you find a 15 cm diameter homogenously erythematous rash on their back. You're done - 2 weeks doxy 100 BID, and go see the next patient!

But what about a test, "just to make sure?" Hey, we're always getting tests. We order BNPs on patients who are on BiPAP and getting 400 µg/minute of nitro, we get a troponin on the patient being rushed to the cath lab for anterior "tombstones," we get a white count in, well, everyone. So why not order a test for Lyme?

Because they don't work well. Some of the pitfalls are:
  • In early localized disease (i.e. EM) about 50% of patients will not yet have a rise in IgM levels.
  • About 5% of the population can  have a positive ELISA test at any given time.
  • In the absence of a supportive history or clinical signs, a positive IgG just indicates past exposure.
  • Elevated IgG, and even IgM, levels can be seen for a long time after successful treatment.
If the rash is equivocal-looking, you can get active and convalescent assays, but this is not routine, and should require discussion with the PMD.

And I enjoy trying to page PMDs almost as much as I enjoy this new yogurt flavor!

#3 Lyme carditis
An otherwise healthy 35 y.o. male comes to the ED with severe presyncope, after having been found to have a heart rate of 30 in the walk-in clinic. He admits to having been told by a coworker at his landscaping job that he had a big red rash on his back 3 months ago (in July), but he never saw it himself. The blood pressure is 80/40, and the ECG shows a complete heart block with a narrow QRS.

How bad is this? I mean, complete heart block - yikes. What should we do right now? Does he need a permanent pacemaker? Will the echo show a nasty cardiomyopathy? How bad is the mortality?

Ok, in order:
  1. Not that bad. These blocks usually last under a week, once antibiotics have been started.
  2. Not a question... But AV blocks are very common in Lyme carditis - about 50% of patients.
  3. Put on pacer pads, order some ceftriaxone, and don't let him walk to the bathroom!
  4. Unlikely. Permanent conduction defects are rare, even though some folks need temporary pacing.
  5. Maybe in the short-term there can be some "reduced squeeze," but the long-term prognosis is very good.
  6. Almost unheard of: a recent review only found two case reports that plausibly link a death due to Lyme disease
Lastly, atropine is not felt to do much, good or bad.


#4 Prophylactic Doxycyline
If a deer tick has been for at least 36 hours, and the patient can take antibiotics within 72 hours after tick removal, and we're in Connecticut (i.e. a Lyme endemic area), the the patient should get doxycyline 200mg PO once.

There are a few wrinkles in this, however. For example, you can't do this for kids - there is no data for prophylactic-dose amoxicillin. 

But most importantly, you have to know the risk-benefit numbers. First, what is the risk of developing erythema migrans after a tick bite, and how much does doxy help? The key NEJM study found:


It looks like most deer tick bites, even in Westchester, NY (a Lyme endemic area), do not result in EM. The risk tops out at about 10% for a somewhat engorged nymph, and plummet for the other categories. The one-time dose of doxy drops that rate down to a little over 1%. That's a pretty decent benefit.

Well, how about the risks of prophylactic dosing? 


A 6% risk of vomiting, and 7% abdminal pain? Hmm.

So, another way of looking at it, the patient potentially has a 90% chance of having nothing happen (if no prophylactic dose), versus a 6% chance of being sick as a dog from the doxy. That's the choice!

The Bottom Line
There's a big fear about Lyme disease in Connecticut, and plenty of people work hard every day to make sure that the paranoia doesn't die down.

Like one of our senators, who investigated and sued the Infectious Disease Society of America
(spending at lot of CT tax money in the process), and was ultimately 100% in the wrong. ***
So, as an emergency doctor in this wacky state, you should know this disease pretty well, so you can identify and treat "Lime's disease" appropriately. You can download the excellent IDSA guidelines for definitive information, or check out the CDC website for clinicians as well.

___________________________________________________________
***  My own political views are not represented here, just a medical perspective. So, in order to balance out my criticisms of a Democrat, let me point out that no political party has a lock on pandering to the "chronic Lyme" folks. To highlight a recent example:


He planned to "improve synergy" in treating Lyme. Cool.


Friday, March 29, 2013

Symptoms in men & women during PCI ballon occlusion

The trouble with "chest pain" is that it's, well, pain. The experience is subjective, bound up in the context of prior experience, current emotional state, and comorbidities, as well as the actual nociceptive stimulus. 

Not Garfield.
Frankly, this complex topic does not get any simpler when we consider the question of whether men & women report significantly different symptoms during ACS

First off, I harbor some skepticism about whether such a significant difference exists at all. For all the talk of "men present typically, women present atypically," there isn't a great deal of evidence that women have substantially different symptoms with pancreatitis, pulmonary embolism, CVA, or even appendicitis. Why should the heart be such a radically different organ? 

Nonetheless, the latest big study on the subject suggested that the rates of "chest pain-free" MI are different between the genders: 31% of males versus 42% of females. However, this was a registry study, with all the usual limitations, and so questions remain. But what can you do? It's not like you can take a group of women, a group of men, give them both MIs, and record their symptoms...

Or can you?

"Gender Differences in Symptoms During 60-Second Balloon Occlusion of the Coronary Artery"
Well, sort of.

Japanese researchers decided to approach this issue prospectively. They enrolled 110 men and 80 women who were scheduled to have PCI for stenting of a single stenotic native coronary artery. None of these patients were having any active symptoms (let alone a STEMI) prior to undergoing PCI. They figured that since the balloon inflation required to deploy the stent causes, essentially, a transient total occlusion, it might prove to be a good model for demonstrating the different symptom expression between genders.

The men and the women were fairly well matched, with the exception that the women were, on average, older than the men. The rates of comorbidities, as well as the target vessels, were similar, however.

 

The duration of balloon inflation during the PCI was standardized at 60 seconds, and the patients were interviewed immediately after balloon deflation for:
"presence or absence of the following symptoms during the balloon inflation: chest pain, toothache, jaw pain, neck/throat pain, shoulder pain, upper or lower arm pain, epigastralgia, occipital pain, back pain, dyspnea, nausea, and vomiting."
The first interesting point is that not everyone had chest pain when the balloon was inflated. In fact, 38/110 men (35%) and 28/80 (35%) women had no symptoms at all.

So, the genders were evenly matched for "pain-free" coronary occlusion. What kind of symptoms did the remaining 65% of men and women have?


Surprisingly, essentially all the men and women reported having "chest pain." When asked about additional symptoms, however, women reported more of the "non-chest" symptoms than did the men, although none of the individual elements reached statistical significance.

To summarize: Men and women had the same rate of symptom-free coronary occlusion, and the same rate of chest pain. Women had more symptoms on top of that chest pain, however. The researchers concluded, nevertheless, that:
[N]on–chest pain symptoms during the 60-second balloon occlusion of the coronary artery were more common in women than in men, supporting the presence of the gender difference in myocardial ischemic symptoms.
Discussion
I think we're making a mistake by focusing on a putative 11% difference in "typical" chest between genders, and should instead remind ourselves that 31% - 42% of patients with ACS do not have a typical presentation. In other words, the variation in symptoms between genders is dwarfed by the range of presentations within either gender.

Furthermore, the present study suggests that the difference in symptoms between men and women, when examined in a fairly well-controlled setting, may be trivial. These results are similar to those obtained by a Canadian group in 2011. Those researchers also employed a PCI setting to record patients' descriptions of symptoms during inflationOverall, they also found no significant difference between the genders.


Now, what do EM residents really want from the review of a new study? They want to know - Can you use the results of this study in the ED tomorrow? And the "trick answer" is that no special gender-based strategy is need or even helpful
 Just be concerned about ACS in everyone!