Snuffbox tenderness: The D-dimer of orthopedics.

The conventional wisdom goes something like this:

Scaphoid fractures are a huge pitfall in emergency medicine. They can be subtle, and easily missed on the x-ray. If you find any tenderness in the anatomic snuffbox, you need to place a thumb spica splint, and have the patient referred to get a repeat x-ray in 7-10 days.

Bollocks. Pure felgercarb.

In a way, the EM approach to the suspected scaphoid fracture is a lot like our approach to the suspected PE. Based on data from the 60s and before, clinicians believe that a disease is difficult to clinically diagnose, radiographically elusive, and requires maximal therapy to avoid devastating outcomes. Some believe that new technologies and tests will provide an solution.

Maybe. But before we try to spend and irradiate our way out of this, let's take a step back, and look at some clinical wisdom you may not have heard about. Research that questions the "conventional wisdom."

And what better fount of conventional wisdom is there, than UpToDate? Let us examine some of the standard clinical advice from the article "Scaphoid Fractures."

Myth 1. Snuffbox tenderness is the cornerstone of diagnosis.
At Yale, there is no shortage of tweed-wearing attendings who solemnly intone rubbish about the decline of the physical exam, about the master diagnosticians of yesteryear, blah, blah, blah...

Cute. Now let's actually look inside.

Hey, you know why we use the ultrasound? Because the physical exams for AAA, CHF, peritoneal blood and gallstones aren't so good, that's why.

Uh, better stop tapping.

Many clinicians cannot recall any other test for scaphoid injury aside from snuffbox tenderness, and this isn't good, because the physical exam is key in determining your clinical suspicion here. This is also a problem since snuffbox tenderness is a lousy test, by itself.

UpToDate, however, assigns it a central role, despite having mentioned other exam techniques (my emphasis):

"Scaphoid fractures are often occult and a high index of suspicion should be maintained for any patient with wrist pain following trauma. Any tenderness in the snuffbox should be treated as a scaphoid fracture until proven otherwise."  (UTD)

This is unfortunate advice, since snuffbox tenderness, while usually very sensitive, is utterly non-specific. Parvizi 1998 found it to be only 19% specific, while Pillai 2005 only found 7% specificity!  Grover 1996 found 29%, and Freeland 1989 must have had a very light touch, determining a specificity of 40%. This makes the d-dimer look good.

With these shortcomings in mind, there are two other important exam techniques you should know:

• Axial compression/impaction - Pressure is exerted in-line with the extended thumb, towards the radius. 
• Tubercle tenderness - Palpate the bony prominence found on the distal flexor crease of the wrist. It is especially pronounced when the wrist is radially deviated and extended.

These aren't just "nice to know," or for historical interest. They might keep you from needlessly working patients up for fractures they don't have.

For instance, tubercle tenderness can be much more specific for fracture, but just as sensitive, according to Freeland 1989 and Parvizi 1998. Along the same lines, Grover 1996 found that the axial compression test was 80% specific, and 100% sensitive.

Parvizi 1998 found, in fact, that requiring a patient to be positive for all 3 exams would still be perfectly sensitive, while boosting specificity to 74%.

Myth 2. Despite negative intial x-rays, 10-25% of patients will have occult scaphoid fractures.
This actually phrased as

"[Splinting] of symptomatic patients with negative x-rays ... may result in approximately 75 to 90 percent of patients being immobilized for a week or more, [needlessly]." (UTD)

 Twenty five percent is a high number, and certainly would justify wrist immobilization if there's any doubt about the diagnosis. It would suggest that radiography is practically useless to detect fractures.

Except that Grover 1996 found that, of the 29 patients who had a scaphoid fracture in their series, all but one was picked up on the initial set of x-rays. Pillai 2005 only had a 7% rate of "occult" scaphoid fracture, while Duncan 1985 saw that none of their 108 patients had an "occult" fracture on follow-up.

So, your mileage may vary, but if both you and the radiologist don't see a fracture, you can feel pretty good about that.

Myth 3. If you don't immobilize the scaphoid soon, there is a huge risk of devastating complications.
The problem with a missed fracture is that non- or mal-union may cause the scaphoid to necrose, which leads to terrible functional outcomes. This is not rare, and it has lead to the perception that immobilization of the wrist needs to take precedence over all other considerations, such as cost, time off from work, and discomfort.

"[N]onunion rates can reach 40 percent when diagnosis and treatment are delayed by four weeks."(UTD)

The reference for this statement, Langhoff 1988, looked at a series of 289 scaphoid fractures. While there was an overall rate of non-union of 3-9%, they found no increase in this rate if the wrist was immobilized up to 28 days following the injury. On the other hand, after 28 days the rate of complications went up. The authors went on to conclude (my emphasis):

"As fractures not visible at the primary X-ray examination were identical with the rest as regards localization and healing characteristics, we assume that these fractures will behave in the same way when subjected to a delay of immobilization of less than four weeks. We therefore consider it unnecessary to immobilize the wrist when there is clinical suspicion of a fracture, but it is not demonstrable at X-ray examination."

They do consider it appropriate to obtain repeat x-rays at 2 weeks if clinical suspicion exists, and forgo immobilization until then.

Myth 4. The presumed scaphoid fracture must be immobilized in a thumb-spica splint.
Well, if my first 2 points are true, this is redundant. But for the sake of argument...

"When a definitive diagnosis cannot be determined at presentation and a scaphoid fracture is suspected on clinical grounds, even if radiographs are negative, the patient should be placed in a thumb spica splint or preferably, a thumb spica cast until a definitive imaging study can be performed." (UTD)

This is a pain in the ass to apply, and probably even worse to wear for the next 10 days, while you try to get into ortho clinic. Good luck using your hand for anything beyond a regal wave.

Hello!

Clay 1991 looked at patients with radiographic fractures, and randomized them to either a "Colles" cast, with the thumb waggling free, or a standard thumb spica.

The nonunion rate was the same in both groups.

Okay, maybe we don't need to immobilize the thumb. But surely we need a hard splint of some sort!

Eh, maybe not. Sjolin 1988 randomized patients with a clinical suspicion for scaphoid fracture, but negative x-rays,, to receive either a dorsal splint (no thumb immobilization) or a "supportive bandage" that could be removed for ADLs.

Everyone got rechecked in 2 weeks, and while there was no difference in complications (all fractures were incomplete or small avulsions), the bandage people were able to go back to work a lot sooner.

And residents need to be able to use their fingers!

Distinguishing STEMI from LVH on the ECG

I've started saying really something annoying at work.

When a resident starts interpreting an ECG, listing off features that either suggest or weigh against active ischemia, they will invariably (and properly) mention the deviation in millimeters of ST segments. I will then sanctamoniously intone

"Amateurs measure millimeters, professionals interpret the whole ECG."

If you think I'm smug about ECGs, ask about my thoughts on Huey Lewis.

Despite the my pretentiousness, there is an important element of truth there. (Dr Smith makes this point without smugness, but that's no fun. For me.) If you slavishly follow the standard criteria for STEMI diagnosis on the ECG (with so-and-so number of millimeters in this lead, so many leads with such elevation, etc.), you're going to make a lot of mistakes. 

One example is LBBB, a very common etiology of STE on the ECG. Usually, of course, the LBBB is immediately identified, owing to its characteristic appearance, and discussion switches to old vs new, and a review of Sgarbossa vs Smith criteria (peer-reviewed video lecture!).

The Problem with Left Ventricular Hypertrophy

Left ventricular hypertrophy (LVH), however, may not be as obvious, and ED physicians may mistakenly activate the cath lab based on the degree of ST segment elevation. Now, mistakes happen, and we want to have a certain "over-triage" rate, just like surgeons (before the use of CT scanners) had to have a certain "false appendectomy" rate. 

LVH, however, is very common, especially in the ED patient population. In fact, LVH is found in about a quarter of the ECGs in the ED that show STE, and is the most common cause.

Brady 2001

And it looks like emergency physicians get fooled by LVH fairly often. In one study of cath lab activations, it was found that LVH predicted a "false-postive" result, with an odds ration of 3.1.

How do we keep from getting fooled by this harmless (in the short-term) mimic of STEMI? It isn't simple. Indeed, one recent article suggested that "novice interpreters" of ECGs avoid diagnosing a STEMI in any patient with deep R- or S-waves.

Don't do it!

Well, I hope you are aspiring to more than "novice" status. I also hope that I can provide you some guidance beyond my usual semi-mystical injunctions and platitudes. 

"Be the ECG, Danny"

The Article

"Electrocardiographic Criteria for ST-Elevation Myocardial Infarction in Patients With Left Ventricular Hypertrophy"

Fortunately, there are non-novice ECG interpreters out there who want to share their secrets, like this group out of UC-Davis. The authors used  a database ("ACTIVATE-SF) of all the emergency physician-initiated cath lab activations over a period of 3 years in the San Francisco area. This gave a denominator of 411 activations.

Applying any of 3 different scoring systems (Cornell, Sokolow-Lyon, or aVR > 11mm), they found that 79 of these patients met ECG criteria for LVH. Now, some of these patients with LVH ended up having culprit arteries identified at angiography, but most didn't. 

They went further, and analyzed this select group of patients who had LVH and a positive cath. They found a few predictors on the ECG.

Certain locations of STE, the degree of STE, and the number of leads with STE all increased the odds of a true STEMI. So did the presence of Q-waves or reciprocal ST depression.

Now, LVH usually only gives you a pseudo-STEMI appearance in the anterior leads, so elevations in the inferior leads, for example, won't cause much confusion. You can see from the table above that STE in the inferior or lateral leads, or a true posterior STEMI, will be easy to distinguish. But what we really care about is trying to distinguish an anterior MI from LVH, and the data above confirms the difficulty; STE in V1-V3 was more often found to not have a culprit artery.

ST Elevation: Absolute and Relative
 Rather than just measuring the absolute amount of STE, however, the authors also analyzed the relative amount of STE, normalized against the difference of the preceding R- and S-waves. 

% STE = (Height T-P segment to J-point) / (Height of R-wave minus depth of S-wave)

Here is an illustration of applying this, using an example of LVH without STEMI from the paper:

True STEMIs, overall, had a higher percent STE (25%) versus "false" STEMI (9%).  More importantly, if the percent STE < 25%, STEMI was essentially ruled out. If the percent STE > 25%, a STEMI was predicted with a sensitivity of 77%, and 91% specificity. 


When they compared this rule, using relative STE, versus the conventional criteria for STEMI that use absolute STE, they found it to be more sensitive and far more specific (73% and 58%, respectively).

Examples
For example this patient has LVH, and STE in V1-V3:

But they also have a ratio of STE/(R - S) = 45% STE

Indicating that it's a true STEMI.

Contrast this ECG with this patient with LVH:

They have STE, just like the preceding patient, but a closer look at the anterior leads shows...

 

... a fairly insignificant STE/R-S ratio, suggesting no active ischemia.

Putting it all together...

For practical use, the authors summarized, in an algorithm, the practical use of their findings, when interpreting an ECG with ST segment elevations.

The Bottom Line

Even if you don't crunch the numbers, try to appreciate the pattern, the proportionality, of the elevations and deviations. You need to look beyond the numbers, feel the waveforms, you need to...

Ah heck, I did it again.

The IMMEDIATE trial: Should EMS give Glucose-Insulin-Potassium?

The results of the IMMEDIATE trial have been popping up repeatedly today on Facebook, partly because I "like" a few EMS FB pages, and also because one of the authors (Hi Carin!) is a FB friend and recent Yale ED attending.

Here's an example of the way the trial is being described:

"ACS patients benefit;" "cut the risk of death in half." Sounds great! I love medical reporting/press releases. No pesky nuance or qualification. Me no need anyhow.

The result they are describing, to be specific, is that 8.7% of the people getting the placebo had a cardiac arrest, or died while they were hospitalized, while only 4.4% of the patients getting the study drug did. That's either an (absolute) difference of 4.3%, or about a (relative) 50% decline.

Such an effect would be stunning.  In the years after thrombolytics and aspirin were introduced, the incremental benefits of new therapies for AMI have been getting smaller and smaller. This result here would blow the others out of the water.

For instance, back in 1988, it was shown in ISIS-2 that either the use of aspirin or of thrombolytics reduced the risk of death in MI by about 2-3% over placebo. The combination was better of course.

After that, it's been harder to show that the more complicated and expensive therapies save that many more lives. When we send a patient to the cath lab for an AMI (instead of giving a thrombolytic in the ED), for example, there isn't that huge a benefit. One recent analysis suggested that, overall, you could only find a 0.7% difference in mortality (6.6% vs 5.9%) between lysed patients, and those that went for PCI. A lot of money for not much gain.

So, if this combination of glucose, insulin, and potassium (GIK) could cut mortality in AMI from 6.6% to, say, 3.3%, it would be freakin' amazing.

"I bet there's a catch. There's always a catch."

Well, I don't mean to be an Eeyore, but the perhaps we should wait for, yes, "further study." I offer three reasons why:

1. They weren't studying mortality.

The principle outcome they were studying was whether the initial presentation of ACS would progress to an MI, or it would be an "aborted" MI. This is the outcome that they believed had the most biochemical and clinical justification, and they clearly thought that it had a reasonable chance of being demonstrated.

It turns out there was no difference in the percent of people who progressed to completed MI - the GIK infusion did not help, at least not here. So the trial is negative for the real primary outcome.

2. There were 12 secondary outcomes.

Look at the table of the results:

Remember: the outcome they staked the success of the trial on was the one at the top: "Progression to MI," for all participants.  The rest are a bunch of secondary outcomes, and they don't count to the same degree as the primary outcome.

Analogy: A friend is flipping a coin, and you call heads. That's your primary outcome of interest. But if you also say to your friend "Okay, I call heads, but I also call it if you drop the coin, if it flips over 5 times in the air, if your phone rings in the next 30 seconds, or if your nose starts to itch in the next 10 seconds.

Now, you may be wrong about heads, but say your friend's nose does indeed start to itch in the next 10 seconds? Will he concede defeat? What will he say?

"No pick! NO PICK!" 

Most likely your friend will point out that the most relevant and important prediction you made was heads vs tails. Furthermore, you called out such a long list of other items that you were almost certain to come up with a positive result. He will insistent on another coin toss, where the primary outcome is now nose-itching, not heads or tails.

The same holds in statistics and study design, and is also why the authors state in their conclusion (my emphasis):

"The primary end point was not significantly different between groups, and the observed favorable results of GIK were based on prespecified but secondary end points, although biologically plausible and consistent with preclinical studies. The study tested one primary hypothesis, 3 major secondary, and 6 other secondary hypotheses. All were prespecified and no adjustment for multiple comparisons among the secondary end points was made; thus, reported significance levels should be considered approximate. Accordingly, given the lack of complete consistency of the findings, and the modest P values for most of the statistically significant findings, it would be appropriate to describe the observed favorable effects on the secondary outcomes as generating clinically testable hypotheses for evaluation in larger cohorts."

3. 30 day mortality seems pretty important too...

Ok, say you can take the "cardiac arrest or in-hospital mortality" results at face value. What, then, shall we make of the 30-day mortality? It was shown to be basically the same in both groups.

We just saw this discussion take place last month. A study from Japan showed that giving epinephrine in cardiac arrest got people to the hospital with ROSC more often, but the 30-day mortality was no different (We'll leave the neuro results alone for now.).

It would be nice if epi put all the dots on the right side of the graph. But it doesn't.

So, say the results are right - people don't die or arrest in the hospital as often, but they still die in the first 30 days just as often. Now, maybe everyone's hospital stay was over 30 days, but I doubt it.

Still feel excited?

Bottom line:

If they conduct another study that confirms the mortality benefit, it would be the greatest thing since the free coffee machine in the ED break room. But, unlike the coffee machine, such results are conjecture for now.

Dextrose for cardiac arrest

Meir and I were talking during a recent shift, and he asked the perceptive question "What's the deal with giving dextrose in a cardiac arrest?"

Good question!

You know that there's a lot of controversy about how to run a cardiac arrest - intubating or not, how often to ventilate, or doing a short trial of CPR before defibrillation. This is especially true regarding the "code drugs," like epinephrine. 

Well, okay. Epi works.

But at least when it comes to epinephrine and amiodarone, there are some studies out there, some base of evidence to start the discussion from. This is not true for D50.

If you look in the 2000 ACLS guidelines, you'll see the list of the "reversible causes" of cardiac arrest. It doesn't include hypoglycemia.

If you don't believe me, look at the fine print at the bottom.

Now skip ahead 5 years, and we now see that hypoglycemia has been added (2005 ACLS):

Down in the green box, at the bottom.

Read through the guidelines, though, and you'll see that not a word is uttered about why this was added.

Now, fast-forward to 2010, and they've taken it out! And, just like they added it without comment, it's gone without justification or evidence, nor even a mere "clinical evidence suggests."

Poof!

Since the AHA elected not to review any relevant evidence about the topic, I decided to answer some questions about hypoglycemia, cardiac arrest, and the relative benefit of trying to squeeze that huge syringe of syrup into an IO.

1. Does hypoglycemia cause cardiac arrest? 

You figure this would be easy enough to answer, but there is almost no direct data that suggests hypoglycemia is a cause of cardiac arrest, let alone a treatable cause.

One case series in 1995 reviewed 3 arrests that the authors thought were associated with hypoglycemia. These patients all had significant primary problems (active CAD, cerebral hemorrhage, and severe pancreatitis), so it's hard to assign blame to the blood sugar.

Another case series, looking at patients with severe heart failure, concluded that one cardiac arrest was due to hypoglycemia (oddly enough, she didn't have diabetes). And in one last example, a patient in the ICU became asystolic at the same time her blood sugar was plummeting, although she also was developing a severe hyperkalemia at the same time.

The problem with this handful of case reports is that, given the uncontrolled nature of the situations, it's hard to point out cause and effect. Just because one thing occurred at the same time as something else, or even right after, doesn't mean they're related.

Well, look at this from a different point of view. Is there a proposed "mechanism," some physiological theory, that suggests that hypoglycemia could cause an arrest?

There is the phenomenon of the "dead in bed" syndrome, where a relatively healthy diabetic is found deceased in the morning. A number of researchers think they've found a link - the usual dip in blood sugar levels at night can cause a prolongation of the QT interval. And long QT intervals can sometimes cause problems! (See these examples at Dr. Smith's ECG Blog.)

A long QTc. (source)

They've been able to show this effect both in the lab (giving insulin to healthy people) and at home (people on continuous ECG and glucose monitoring).

But, just because you can show a longer QT, doesn't mean you have a smoking gun! Others have pointed out that there are probably a number of other factors involved. For instance, it may not be the hypoglycemia that triggers the QT changes, but in fact may be the body's own epinephrine that kicks off the arrythmias!

Now epinephrine is bad for the heart?!?

So, we just don't know.

2. Is the finger stick accurate in cardiac arrest?

Usually, the capillary blood glucose is pretty close to the venous level, close enough that we all trust it. However, in the critically ill patient, the capillary level becomes less accurate, as a number of studies have shown.

Only one study has looked at patients getting CPR, though.  This was a pretty big study by cardiac arrest standards - they checked the venous and capillary glucose levels in 50 cardiac arrest patient. It wasn't encouraging.

There were 4 patients with "true" hypoglycemia, found on the venous samples sent to the lab. The fingerstick missed 1 of those, and also managed to misdiagnose 5 patients as having hypoglycemia, when they really didn't. (That works out to 75% sensitive, and 38% specific).

Not so useful. So, perhaps we should just skip testing, and treat empirically. What could be the harm in that?

 3. What's the harm in empirically treating for hypoglycemia?

Glad you asked.

It's the same reason we're trying to cool people down after we get a pulse back  - neurologic outcomes. In some studies, they gave dextrose to some cats before they put 'em into cardiac arrest, while other cats they didn't. The cats who didn't get sugar beforehand had better brains afterwards.

You can't really do this same kind of study in humans (for example). One group in Helsinki, though, checked the blood sugar on VF cardiac arrests, and looked at how well they recovered. Patients who had increases in their glucose after resuscitation didn't survive to hospital discharge as often. This is just the latest evidence - see this review article (50% dextrose: antidote or toxin?) for plenty of other examples.

4. Any evidence giving sugar helps? 

Well, yes and no. There is no evidence that pumping liquid rock candy into someone's tibia helps in cardiac arrest.

Medicine!

Now, there are a lot of other sick people out there, people teetering on the edge, critically ill, septic, metabolically deranged - with a blood sugar headed south, and fast. You have to find those folks and treat them quick. Some of these are kids, with weird metabolic problems, or with sepsis.  But the key is to get to them before they crash, while they still have a pulse.

The authors of the only review I found on this topic concluded that (my emphasis):

"This is obviously a controversial issue and raises the point of whether we should still be teaching that hypoglycaemia is a reversible cause of cardiac arrest when there seems to be not enough evidence to support this. 

Current evidence would suggest that patients may suffer cardio-respiratory arrest with hypoglycaemia, but not because of it." 

The Bottom Line

Despite the huge crowd in the room whenever a patient is "coding," there are only a limited number of spaces around the patient. Likewise, you have the contents of the whole code cart available to you, but can only push each drug one at a time. You have to pick your priorities in a code, and it doesn't appear as though pushing sugar water ought to one of those.

Procainamide - Hipster drug, or too mainstream?

I recently gave procainamide to a patient in the ED. It was a big fuss - we had to send a runner to the pharmacy, the nurse had to blow the dust off the administration protocol. Great fun.

Later on I was describing this to another ED attending, and one of the senior trauma surgeons, overhearing this, exclaimed "You're not old enough to give procainamide!"

He proceded to launch into an Abraham Simpson-esque tale about long-lost antiarrhythmics, and I sort of lost the point of his story...

"... which was the style at the time...

Anyway. The point today is that procainamide is back, and we should be thinking of giving it far more often than we do.

For example, with...

Stable monomorphic ventricular tachycardia

Yet another "chest pressure and palpitations gets rolled into major med. He looks good, no acute distress, joking awkwardly with the techs as the monitor leads are attached. You dutifully punch in the orders for a chest x-ray, troponin, etc., when you notice this on the monitor.

"Is he just shaking real bad?"

Ah. Well, it turns out that his vitals are just fine, and he looks stable enough, but you could use "synchronized cardioversion" to fill out your procedure log. Unfortunately, he just ate a couple burritos on the way over. That's going to make procedural sedation a little dicier, so perhaps you'll try a medication. But which one?

On the one hand, there's amiodarone, which seems reasonable, given how often it's given in the ED. On the other hand, lidocaine is readily at hand.

Dose: Give 1 box.

Well, the AHA thinks that procainamide is likely your best bet here. Just sayin'.

Dose: "It's complicated."

In the 2006 AHA Guidelines for the Management of Ventricular Arrhythmias, makes a few suggestions. First of all, if it's unstable, shock it!

If it's not, the evidence is best (level B) that procainamide converts VT more often than anything else. In one trial procainamide terminated 38/48 episodes of VT - not as good as electricity, but pretty good!

They do recommend amiodarone for the patient who is unstable and has failed cardioversion, and in whom the other drugs aren't working either.  One reference that the guidelines cite in support of using amiodarone describes evidence that "demonstrated a dose-response relation, with at least comparable efficacy to bretylium."

Yes, at least as good as a drug that was taken off the market years ago, and didn't even work for E.T. Sweet.

"Uh, better grab the Glidescope.  I think."

Conversion of atrial fibrillation

You got a 40 year old guy in the ED, who says that he started having strong palpitations about 2 hours ago while at work. No recent drinking, no drugs, but he does quite a bit of running, however.

A healthy patient with a clearly defined time of onset - a great candidate for ED cardioversion! You get the pads, set up the airway gear, and calculate the propofol dose. As you consent him, however, you learn that 30 minutes ago he wolfed down one of these:

Those darn vicious burritos.

Crumb. That's not going to look so great going down his right mainstem. Well, how about drugs?

Well, amiodarone seems to be the default choice. The 2006 AHA guidelines seemed pretty bullish on amio, giving it a Class IIa rating for conversion of AF, relegating procainamide to a measly Class IIb.  The funny thing is, their summary of the utility of amio in AF is not exactly inspiring. They describe trials of amiodarone that show it to be "no more effective than placebo," and "more effective than placebo after 6 to 8 h and at 24 h but not at 1 to 2 h." 

They relegate procainamide to the list of drug that are "Less Effective or Incompletely Studied," which has to reflect a little anti-north-of-the-border bias, given that the Canadian cardiologists had already looked over the world's literature, and come to a different conclusion.

When Canadians want to convert AF in the ED, they reach for procainamide. In the 2010 Canadian Cardiovascular Society Atrial Fibrillation Guidelines (also here as a PDF download), our Canadian brethren ranked the best drugs for conversion of recent-onset AF:

"Amio has to be here somewhere..."

One trial was used to cite the effectiveness of procainamide in AF (happened to be a Canadian paper, but published in a U.S. EM journal), showing that it converted about half of the patients. They don't cite other papers, but past results (from 1983 and 1993, for example) could also be used to support the guidelines. One recent trial (done by the same Canadian) showed a 60% cardioversion rate.

Canadian cardiologist, showing their pride with a tattoo on their...  Ok, what body part is that?

Wide complex atrial fibrillation, possible WPW.

So, by this point, you're a wiz at terminating VT, you've mastered the art of atrial fibrillation - there is nothing can triage can do to hurt you.

Fifteen minutes before the end of your shift, they roll in a middle-age women with "palpitations." No problem for a boss like you - you'll have major med tidied up for sign-out in no time.

"Challange Accep... Geez, is that her ECG?"

The tech hands you this ECG:

Her blood pressure is fine, and she doesn't look too symptomatic. She tells you that she has some "extra wires" in her heart, and that she gets spells like this sometimes.

Sooo, irregular wide-complex tachycardia. This could be WPW with atrial fibrillation, so your therapeutic options just narrowed. No metoprolol, no diltiazem. Again, it would be great to cardiovert her, but she doesn't want to consent for that.

Gosh, what medication would work best here?

Well, it ain't amiodarone. That drug has been out of favor, for this situation, for some time. Mel Herbert, of EM:RAP fame, published a review in 2005 entitled "Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department"

The title pretty much explains the conclusions, but they also concluded that, while amio was the worst of the bunch, electricity was the "only therapeutic modality lacking pro-arrhythmic properties."

Of course, this was old news in some quarters. The 2003 AHA Guidelines for the management of patients with supraventricular arrhythmias was not bullish on amiodarone, and  mentioned only the use of procainamide, ibutilide, or flecainide for chemical conversion of AF with WPW.

So it was not a suprise when the AHA updated the atrial fibrillation guidelines last year, and bumped procainamide up to a Class I recommendation for AF in WPW. Amiodarone is still okay to use, but it is class IIb - weak!

Bottom line

Brush up on your dosing, cuz' this drug is back like horned rim glasses - so old fashioned that it's back in style.

But seriously, review the dosing, because it's a bit more involved than "give 1 vial." Also, it's totally fair "pimping" material!

"Women present atypically."

A recent study got a bit of press, and it got me to thinkin'. Specifically, it got me to thinking about those clinicians who  say stuff like "Women typically present atypically," and stuff like that. Like they're a whole other species when it comes to matters of the heart.

Now, I was going to go through the results, look at the past literature, put things in context... Boring! The heck with that - I'm going in a different direction.

I figure that if women are so different from men when it comes to ACS, then they must have different symptoms with a bunch of other diseases as well. Right?  So here goes!

Pancreatitis
Why don't we talk about how men and women present differently with pancreatitis? Both the heart and the pancreas are visceral organs, with indirect transmission of nociception, and are subject to hormonal influence. Although there is a clear divide in etiology based on gender (men drink, women get gallstones), there doesn't appear to be any difference in the symptoms.

Extensive Pubmed and Google searches turned up only one somewhat relevant paper. Unfortunately, they only studied the relationship of patient gender to disease severity, and made no comments about symptoms at presentation.

Bottom line: Absolutely no data in the literature, on way or another. Anybody need a research project?

Pulmonary embolism
So, just like MI, this is a bad one to miss. Just like the heart, the symptoms can be protean and vague, and hormones like estrogen are often implicated. Should be a slam-dunk for a difference in symptoms!

Swiss researchers combined the results of 3 prospective trials, looking at the clinical presentation of 3414 outpatients with suspected PE. When they looked at the all the data, they found that, apparently, women and men presented with about the same symptoms (small exception - men more often had a concomitant symptomatic DVT). Warning - big slug of data here:

Note that men and women both had chest pain at about the same rate - very reassuring! There are some small differences, but aside from DVT symptoms, nothing is statistically significant. In addition, both the Wells and Geneva scores showed comparable performance in both genders.

Bottom line: It's only one paper, but it has a great design.

Stroke
Along with STEMIs and major trauma, stroke is one of the big three time-dependent, resource-intensive, emergency medicine priorities. Now, given that the history and physical exam are so crucial in our evaluation of tPA candidates, it would be good to know if we had to adjust our diagnosis to the gender of the patient. There have been 3 recent studies, with different methods, that all speak to this issue.

Looks sort of sketchy, right? Stuffed animals, adult woman... (source)

Lisabeth 2009 used interviews, asking the patient what symptoms had brought them to the hospital. These interviews were conducted after admission, but despite the potential for recall bias, few differences were found: Only "mental status change" rose to (marginal) significance.

Gargano 2009 was also performed in Michigan, but used registry data from almost two thousand admissions. Instead of interviewers, they abstracted data from ED documentation.

There appear to be few significant differences between the sexes here. Men having slightly more "balance/dizziness" problems than women, which seemed to drive the marginal difference in "Any warning sign or suspect stroke." Even the authors concede that:

 "Overall, the sex differences in symptoms we identified were relatively minor..." 

A Tasmanian study, Gall 2010, also showed some minor differences, but nothing clinically significant.

Women were significantly less likely to have dysarthria, ataxia, or paresthesia at stroke onset than men, but more often had incontinence, loss of consciousness, visual deficits, and dysphasia. ...  Despite sex differences in the prevalence of signs and symptoms, the ranking of the top 5 symptoms was similar for men and women.

Bottom line: Minor differences, of little clinical significance across a number of sites and study designs. Here, at least, men act like women. Or the other way around.

Appendicitis
No only is the hormonal milieu different in this case, but the anatomy as well! With all the added adnexa & "stuff," the differential diagnosis is expanded, and the evaluation, and especially imaging choices, can be quite different for the boys and the girls.

And cylons.  Cylons definitely have atypical presentations.

So it's reasonable to think that the presenting symptoms would be significantly different as well. I only found 2 studies that fit the bill, however, and they have some disappointing shortcomings.

Guss 2000 looked at 196 ED patients who ended up with a diagnosis of appendicitis. Now this is the funny thing - the women had longer diagnostic work-ups before operation, but the men had higher rates of perforation. Apparently, though, they presented in much the same manner:

Oddly, there is no mention of RLQ tenderness here. Although the methods described how tenderness at McBurney's point was to be included, no mention is made in the results. Strange omission...

A similar study was done by McGann-Donlan 2009, comparing 137 men and women, by chart review, who had received a diagnosis of appendicitis. Rather than a surgical diagnosis, the CT scan was taken to be the "gold standard" of diagnosis. (By contrast, only 3 patients in Guss 2000 had CTs!)

Hmm, shouldn't there be some p's kicking around? Perhaps a SD or two, or even, heaven forfend, some confidence interval? Ah, no. Let me quote (italics from the original):

Females more commonly had nausea (66% of females vs 43% of males), vomiting (37% of females vs 32% of males), and diarrhea (18% of females vs 7% of males). Females less commonly had RLQ (right lower quadrant) pain (77% of females vs 88% of males) and fever (1.5% of females vs 7% of males). There was no difference in anorexia between genders (29% of females vs 30% of males)

Apparently italics are the new p-value. Brady, did you already know this?

Now, the problem with these two studies is that they only looked at patients with diagnosed appendicitis - they didn't look at patients with suspected appendicitis.

Eskelinen 1994 took a whole other approach. They collected data prospectively from over a thousand patients presenting with abdominal pain (not just those with confirmed appys), and tried to construct gender-specific prediction models (unlike, e.g., the MANTRELS score). Through multivariate analysis they determined the independent predictive elements for men and women. The elements in the "B" column are the regression coefficients - the higher the number, the higher the weight that element contributes to the score. Comparing men % women, we find:

Well, it looks like RLQ pain is the most important element for both genders. Most of the other symptoms washed out of both models - migration, intensity, anorexia, etc.

Bottom line - There appears to be no consistent, clinically significant difference between the genders in appendicitis.

Lyme
On one hand, you wouldn't expect Borrelia to show up differently in men & women, since it's a freakin' bacteria. What does it know?

That's how B. burdorferi rolls.

On the other hand, this disease was first diagnosed in CT after one mother insisted that her child's disease that was being misdiagnosed. Since that dynamic (i.e. doctor vs lay-woman) is part & parcel of the Lyme disease history, you might expect some gender-based analysis in the literature.

Bingo.


"Sex differences in the clinical and serologic presentation of early Lyme disease" supposedly demonstrates that both women and men have similar symptoms in early Lyme, but have different immune responses. I'm not going to use this paper to prove any points, for a few reasons.

First, the lead author is employed at the Lyme Disease Research Foundation, which is an organization founded & run by the last author, Aucott. In other words, the last author is the boss of the first author.

Boss? Time for a gratuitous picture of my hero!

Second. it's kind of a crap paper. All the Lyme symptoms were diagnosed by 1 doctor - Dr. Aucott.

Last, it has an agenda. Many proponents of "chronic Lyme" believe current immunologic techniques of diagnosing Lyme disease do not work. (This notion, by the way, has no support from people who actually did fellowships in ID.) The paper here will likely be used to suggest that such tests discriminate against women, even in early disease. They're using the shield of "gender-based medicine" to advance their chronic Lyme agenda. For example:

(The lead author, Stricker, has had an article retracted from the NEJM for falsifying data. Not a trustworthy doctor. Nowadays he's an expert on Morgellons.)

Okay, now I'm ranting. Time to wrap this up!

Conclusion
Whatever your take on the cardiology literature is, I found little evidence that demonstrated that women evince significantly different symptoms than men in a number of other acute diseases.