"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.

Intubation and Mis-en-place.

Back when I was a paramedic-wannabe, one of the experienced medics showed me his elaborate way of arranging his equipment at the start of the shift, including where he placed pre-torn pieces of tape, ready at a moment's notice to secure an IV line. He called this process "tape karma." It was a catchy phrase, and I respected his ritualistic attention to preparation.

In a similar way, line cooks in restaurants prepare for the chaos of a Saturday evening rush by meticulously preparing their station. The arrangement, known as mis-en-place (Roland can help you out with pronunciation!), is personal and exact; ingredients collected, utensils readied, and stations cleaned. As per Anthony Bourdain:

What exactly is this mystical mise-en-place I keep going on about? Why are some line cooks driven to apoplexy at the pinching of even a few grains of salt, a pinch of parsley? Because it’s ours. Because we set it up the way we want it. Because it’s like our knives, about which you hear the comment: ‘Don’t touch my [duck], don’t touch my knife."

Someone messed with the mis. (Thanks Evan!)

If line cooks are going to be fanatical about how they prepare your duck a l'orange, perhaps you should develop your own airway mis-en place. That is, a systematic preparation for each intubation attempt that is ritualistic and practiced.

I submit that these 5 items should form the core of your "airway mis." Add or substitute as you see fit, but regardless, get your mis in gear!

If you let your mise-en-place run down, get dirty and disorganized, you’ll quickly find yourself spinning in place and calling for backup. I worked with a chef who used to step behind the line to a dirty cook’s station in the middle of a rush to explain why the offending cook was falling behind. He’d press his palm down on the cutting board, which was littered with peppercorns, spattered sauce, bits of parsley, bread crumbs and the usual flotsam and jetsam that accumulates quickly on a station if not constantly wiped away with a moist side towel. “You see this?” he’d inquire, raising his palm so that the cook could see the bits of dirt and scraps sticking to his chef’s palm. “That’s what the inside of your head looks like now.”

1. Head elevation:
This simple maneuver is frequently skipped, but can really improve visualization of the larynx. In a person of normal habitus, place enough padding (folded towels or sheets) under the occiput to elevate the head 7 cm off the bed. There are a few ways to explain this, but the best is empiric - it is proven to improve the glottic view. In Levitan 2003, the authors compared the laryngoscopic view with the patient laying flat, with the head up by 7cm, and somewhere in the middle.

The amount of the glottis that could be seen went from about 30% when laying flat, to 80% with head elevation. Now, you can't do this with the trauma patients, but in the medical patients, you're wasting time and left arm strength if you don't grab a folded sheet to shove under the head.

"And teal arrows! Grab me 3 or 4 teal arrows!

2. Ramping:
Now, a little folded towel isn't gonna help you when you're about to intubate this:

Because of all the excess tissue in her lower back, her neck and chest have about the same geometric relationship when she is supine as this lady does...

... in her fancy yoga pose. The red triangle schematically represents adipose, demonstrating how the neck gets flexed in obese patients. You need to get these folks "uncrunched" before you get your laryngoscope ready. You need to ramp them!

The idea is that you create a triangular wedge that elevates the upper back and shoulders off the bed. Once you have corrected the neck-chest relationship, you also have to ensure that you have head elevation as well. In practice it looks like this:

Note how the external ear meatus is level with the sternal notch - this relationship is key to creating good intubating conditions. With significant obesity, a good deal of effort may have to be made to achieve this alignment:

That's a lot of laundry. But, if you've ever skipped this part in an obese patient, and found it difficult to even get the laryngoscope blade in the mouth because the handle was getting caught up on the chest, you'll recognize the wisdom of this approach immediately.

3. Tube & Stylet Shaping:
This only applies to direct laryngoscopy - using the Glidescope requires modification!

The odd thing about medicine is that there can be so little evidence in some areas (hypertensive urgency, anyone?), while there is plenty in other areas, such as how to shape the ET tube and stylet.

There are a number of reasons that an ET tube that is bent in a "hockey stick" form (straight down to the cuff, then bent upwards) improves visualization and placement. There is some variation, however, with how much bend is required. Levitan and pals intubated a few cadavers, using ET tubes and stylets bent into a "hockey stick" shape with angles ranging from 25° to 60°. 

What they found was that an angle sharper than 35° increased the difficulty of tube passage significantly - at 60°, over half of the ET passage attempts were rated "impossible!"


4. Cricoid pressure is misunderstood:

Simply put:

Cricoid pressure ≠ BURP maneuver ≠ Laryngeal manipulation

The two cartilaginous structures are structurally distinct, are attached to surrounding anatomy in different ways, and respond to manipulation in distinct manners.

• Cricoid pressure, in which the cricoid cartilage is displayed posteriorly, is not mean to aid visualization, but to prevent passive regurgitation during RSI.
• The Backwards-Upwards-Rightwards-Pressure (BURP) maneuver employs manipulation of the laryngeal cartilage. It is performed by an unguided assistant, and is intended to improve visualization.
• External laryngeal manipulation (of the laryngeal cartilage) is performed by the laryngoscopist with their free right hand, also to improve the view.

Most importantly, cricoid pressure may be very difficult to apply correctly, and do little to prevent aspiration even when done perfectly. Furthermore, it may worsen the chances of successful intubation. In a review of the risks and benefits of the cricoid pressure (or Sellick's maneuver),  Ellis and Harris reviewed a mountain of literature. This an essential paper for every EM physician, and I'll email a PDF to anyone who wants it. They found that:

• "Recent anatomic investigations on live patients undermine the conclusions of initial cadaver studies validating the technique."
• "Cricoid pressure consistently reduces tidal volume and increases peak inspiratory pressures when applied during bag-valve-mask ventilation, and even controlled, well applied cricoid pressure can adversely effect ventilation and cause airway obstruction."
• "There is solid evidence that cricoid pressure is applied inconsistently in all intubating environments. Indeed, if we are not able to perform it as recommended (ie, without excessive force at the correct location) whether or not it is a useful technique becomes a secondary argument."

They conclude that:

Given that the risks of cricoid pressure worsening laryngeal view and reducing airway patency have been well described, we recommend that the removal of cricoid pressure be an immediate consideration if there is any difficulty either intubating or ventilating the ED patient.

While that review was based on a systematic review of the literature, the same authors then conducted a study of their own, looking at the benefit of switching between cricoid and laryngeal maneuvers during intubation attempts. One table well-summarizes their findings:

CP = cricoid pressure, BLM = external (bimanual) laryngeal manipulation

So, know the differences in these maneuvers, how and when to best apply them, and understand when to switch between them!

5. Pull the Cheek:
So you're almost there - you see the cords, the #8 is in your right and your attending is shouting "What do you see?" in your ear. As you start to send it home, though, the mouth starts looking a bit crowded, and you lose sight of the precious cords. What to do?

Put your attending to work - ask them to pull the right cheek to the side, creating more room to visualize and place the tube.

I tell ya', it's like finding $10 in your just-washed scrubs - free money!

Pitfalls in stroke

Perhaps my recollections of working in Major Med are different than your experiences. When I was up to my ears in patients, spread a mile wide and a centimeter deep, the last thing I wanted to hear was...

WHO CAN COME OUT?

... unless it was immediately followed by "EMS is bringing in a stroke alert!" That meant that a neurology resident would be swooping in, protocols falling in place, and things happening without needing my constant input. 

Perhaps it was wrong of me, karmically improper, to wish that everyone would have their stroke during my shift. Where I work now, the whole stroke team is this guy:

As a result of my new status, I've had to learn a bit more about fibrinolysis of the acute CVA than I did previously. Mostly this has to do with finding exclusions to administering tPA. Clearly, using a check-list is essential here, as well as knowing the policies of your own institution. With that in mind, however, I want to emphasize some pitfalls in the process. For a quick reference to the tPA guidelines, refer to my old post.

Case 1:

EMS calls in with 55 year old female who has had left arm & leg paresis, with a witnessed onset 30 minutes ago. Vital signs and glucose are normal. When you press the paramedics for more information they say that her whole family witnessed the episode. She was seated at the dinner table, but had not yet started eating, when she stiffened up, and then shook for a minute. When EMS arrived she was talking, but she had the new left-sided deficits. 

In the ED, the CT shows no bleed, and so the pharmacy calls down and asks if they should send the tPA with a runner...

Contraindication: Patient had seizure at onset of stroke. 

Or rather, the patient had a seizure at the onset of a "potential stroke-mimic." The concern is that the apparent CVA is actually a Todd's paralysis (pdf), having nothing to do with an embolic or thrombotic etiology. This exclusion has been modified recently, allowing for lysis if imaging can demonstrate an acute vascular occlusion, but this is difficult to achieve in most institutions.

Case 2: 

A 60 year old man is brought in about 2 hours after witnessed onset of right facial droop and aphasia. His vital signs and glucose are normal, his NIHSS  works out to 10, and the CT scan shows no bleed. He take warfarin for paroxysmal AF, but (thankfully?) due to non-adherence, his INR is 1.1. At the 2.75 hours post-onset mark, tPA is started.

Fine - no exclusions.

However, say this same patient was brought in 15 minutes later, and as a result, we are standing over him with the tPA at 3.1 hours post-onset...

Hint.

Contraindication: Oral anticoagulation therapy, even if INR within normal limits.

The ECASS III trial, which provided the evidence to extend the tPA-window to 4.5 hours after stroke onset, had different exclusion criteria than the NINDS-based 3 hour window. Specifically, if a patient will be getting tPA within the 3-hour window, their INR had to be less than 1.7. In the 3-4.5 hour window, though, any use of an oral anticoagulant is an exclusion. 

Case 3:

A 75 year-old woman is brought in with left arm paresis, as well as left side neglect. She was last seen normal 2 hours ago. She does not take warfarin, Other history include HTN and a prior CVA 5 years ago. The CT is read as negative for acute findings, and the labs return at 3.25 hours after the onset of symptoms. After discussion with the neurologist, you start the tPA at 3.5 hours.

Sounds good.

"I forgot the rest of her med list," says the patient's daughter, right before the nurse starts the tPA. Let's see; metoprolol, amlodipine, metformin, Ambien... Wait, what?

Exclusion: Combination of previous stroke and diabetes mellitus

Yeah, I am trying to emphasize that the 3-hour window is not the same as the 3-4.5 hour window. One of the trickier exclusion criteria is the combination of DM and prior CVA - this is why you have checklists! Now, I don't recall the reasoning behind this particular exclusion, but, in general, ECASS III was trying to enroll a healthier cohort than NINDS, and people with both those comorbidities are not likely very healthy.

Case 4:

A 65 year-old male with acute onset dysarthria and left-sided deficits presents within 3 hours, and has a negative CT. Unfortunately (?) he is excluded for receiving tPA for other reasons. The RN notes that his blood pressure is sticking around 200/100, and asks you what you're going to do about it - "They won't take 'em on the floor with that pressure!"

"Drink me."

You reach for the labetalol and say..

"Hey, did you read that recent study in Stroke? There was a great review of the paper on this cool EM blog... We better not give this labetalol just yet."

Me on my days off. I'm a player.

There are a lot of times when we don't want to treat the blood pressure, and this is the prime example. Per the AHA class 1 recommendation in the stroke guidelines:

It is generally agreed that patients with markedly elevated blood pressure may have their blood pressure lowered. A reasonable goal would be to lower blood pressure by 15% during the first 24 hours after onset of stroke. The level of blood pressure that would mandate such treatment is not known, but consensus exists that medications should be withheld unless the systolic blood pressure is >220mm Hg or the mean blood pressure is >120 mm Hg (Class I,Level of Evidence C).

Okay, wait until the SBP is over 220 - seems crystal clear, right? Well, people have a hard time ignoring those pressures, and end up treating them. As this recent study shows, we treat when he don't have to, and then we over-treat, dropping the pressure too far, risking a watershed infarct. 

Okay, I think we get the idea! 

Syncope and Dysrhythmias - Part 1

How come we never talk no more? probably my fault...

Virginia & I had an interesting patient at the 'Port recently. It was the best kind of interesting - lots of EKGs, specialists involved, and no ensuing tragedies. Nice.

It didn't start out promising -  a kid who faints (not feints) is not usually the most interesting patient. Kids faint a lot - exhibit A:

So when EMS patched, saying they were bringing a 14 year old girl who had fainted, it didn't really grab our attention, until they mentioned her heart rate was dipping into the 40s during transport. 

Ah. I see. Meet you in room 4... 

The Patient
During the evening she had been feeling an upset stomach, describing some epigastric discomfort, as well as nausea. Her parents remember that she looked a little pale before the episode occurred. She was walking into the kitchen when she began to feel faint, and fell to the floor. Her parents, frightened, called 911 immediately.

The ALS crew found her sitting up in a chair, a tissue held up to a small cut on her forehead, but otherwise looking well. Vital signs were normal, and the parents were starting to feel like they had been overreacted in calling 911. While sitting in the chair, however, she suddenly stiffened up her whole body, and then went limp. After being put on the floor, however, she regained consciousness. Although she came around quickly this time as well, everybody decided that calling 911 had been just fine, and she was moved to the ambulance for transport to the ED.

During transport, the medic noticed that her heart rate was slowing down episodically, dipping into the 40's. She still looked pale, and vomited a few times, but her mental status was fine, and she never became hypotensive. A rhythm strip was obtained:

An ECG was also acquired:

The transient episodes of bradycardia did not require pacing or medication. She was brought into room 4, looking a bit intimidated by the number of nurses and doctors around her. She still looked pale, but her speech and mentation were normal. An ECG was obtained in the ED (about 30 minutes after the EMS ECG):

Vital signs were P-100, R-20, BP-127/59, SaO2-100% RA. Her lab work was uninteresting, and a CT of her head show no fractures or bleeding. The cut on her face needed only some Dermabond.


ECG analysis
The ECG and rhythm strip obtained by EMS were acquired only a minute apart. The rhythm is interesting, showing a sinus rate of around 120, but with a 2:1 AV block, so that the ventricular rate averages 60. On the rhythm strip we see two episodes of more advanced AV block, with 3:1 conduction, while on the 12-lead we see an apparent Wenkebach pattern in complexes 5-9, with a progressively lengthening PR interval. The QTc, fortunately, appears normal, and there are no signs of pre-excitation, Brugada, or arrhythmogenic right ventricular dysplasia.

The ED ECG shows, first of all, how frakkin' important it is for EMS to grab ECGs in the field, since a number of features had changed on the ED tracing. In the ED there is only a mild 1st-degree AV block (214 ms), and no sign of Wenkebach phenomena. The computer read the QTc as 441 ms, "borderline prolonged," and it does appear to violate the "half the RR interval" rule for a normal QT.

https://www.kg-ekgpress.com/

Hospital course
Our patient was transfered to our local quaternary-care center. She was continued on cardiac monitoring during her hospital admission, but 24 hours of telemetry revealed only a single further dropped beat, as well as a resolution of her PRI prolongation. Tests for Lyme, as well as rarer infectious causes of AV block or myocarditis, were negative. She was due to start a Holter study upon discharge, and follow up with a pediatric cardiologist.

Turns out HIPPA does not apply to dogs, so I can show you a canine Holter monitor.

Discussion

1. Was this a seizure or what?
Although the second episode of syncope this young lady had began with an apparent seizure, it was unlikely to represent  a primary neurologic process. First of all, the seizure was described as a brief whole body stiffening, follow by loss of tone. While some forms of epilepsy may manifest in this manner, it would be unusual. Also, there was no post-ictal confusion described by the paramedic or parents, making a "true" seizure unlikely. Other historical and exam findings also weigh against a seizure. A good illustration of other factors to consider are found in this article "Seizure versus syncope (PDF download), which features a handy guide:

So this was likely a "convulsive" sub-type of syncope (brief myoclonus due to low blood flow to the brain), following the flowchart above. (In some literature, the convulsive type refers specifically to pallid breath-holding spells in children. I mean it more generally here.)



2. Ok, it's syncope - what kind was it?
Reading the textbooks, there are dozens of terms to describe the various supposed kinds of seizures; micturation, situational, vasovagal, neurocardiogenic, autonomic, reflex... you get the idea. Really, there are only two types of syncope out there, from an EM point of view; cardiac or non-cardiac. Let's start with the second.


"Non-cardiac" does, of course involve the heart, but it's role comes in at the end of a sequence of events which are, as usual in medicine, not well worked out. The standard explanation sounds so weird, it may even be true.


For whatever reason, the body can pool blood excessively in the lower extremities. To compensate, both vascular tone and cardiac output increase substantially. Unfortunately, various pressure receptors in the heart now think the body is hypertensive, and act as if the patient has high intercerebral pressure; the heart rate drops, and cardiac output falls.

The fall in heart rate and blood pressure appear to be mediated by the vagal nerve, at least in part, so people call this vasovaagal syncope. On the other hand, since the sympathetic pathway is also affected, others call this autonomic syncope. Of course, as the picture above shows, the brain has a role in this, so it also called neurally-mediated syncope. If bardycardia, or even asystole (transient), are the main manifestations, it may be termed cardioinhibitory, but if hypotension is prominent, it can be instead called vasodepressor syncope. 


Whatever. The important point is to distinguish these benign types from cardiac causes. This kind of "syncope" is caused by a primary problem within the heart, and may not produce all the autonomic symptoms (sweating, warmth, nausea) that normal syncope does. It comes on fast, and can occur even if the patient is seated or supine. This table from a Nadas' Pediatric Cardiology reviews the differences with normal, or "neurally-mediated" syncope:

Remember how normal syncope has a bunch of vague terms to describe the same thing? In contrast, there are 3 distinct types of cardiac syncope, with clearly defined etiologies.


First, there are structural causes (hypertrophic cardiomyopathy, tetrology of Fallot, pericardial tamponade, amongst others). 


Next, tachyarrythmias can induce syncope. Examples include long QT, Wolf-Parkinson-White, and Brugada. 

I calculated 411 msec. Normal.

Last, but certainly not least, we have to worry about bradyarrythmias - sick sinus syndrome, overdose of beta-blockers, and, of course, advanced AV blocks!


3. Finally! So, did the AV block cause the syncope, or vice-versa?

Salma Hayek is always relevant.

Sounds like a good question. I'll discuss that in the succeeding post, as well as the reasoning of the cardiologists taking care of our patient.

Shoulder relocation - Amateur hour!

Sounds like most people have seen the website ShoulderDislocation.net. Great videos, instruction, etc. Can't recommend it enough.

But, frankly, after I've sweated and worked to reduce a shoulder using the Kocher, or Milch, or whatever procedure, and it's going nowhere, watching those videos makes me feel like a chump. Cunningham just waves his hands over the glenohumeral joint, like some sort of Australian Yoda, and Pop! Right back in.

Seriously, how can he do that?! Well, I'm working my way there, but I'm still in the realm of the Padawan, nowhere near Jedi level. So, for some ego-reinforcement, I turned to YouTube! A number of plucky DIY-ers have filmed their own approaches to shoulder reduction, and our self-esteem, if not our board-scores, stand to benefit form viewing their efforts.

In this first, it looks like the "friends" are about to apply the Spaso technique.

Ah, no.

Next, we have another example of the "maybe if we yank harder and faster" technique. The still from 0:03 tells you all you need to know about the context of the therapeutic maneuvers.

Beer? Video camera? No dislocation apparent? Go for it!

Okay, 1 last example of the "Martin Riggs" technique:

Enough negativity. You already feel that you're probably better at shoulder relocation than an inebriated crowd of adolescent males. But here are a few examples of gettin' 'er done that ought to make us feel a little humble!

This guy, likely very experienced and knowledgeable, talks hi friends through a Milch reduction:

This guy isn't quite so astute, but he gets the results he needs:

Again, the yanking. What the frak?

Lastly, this is my all-time favorite. "They just saw it on YouTube!" The reductionists start off with a brief stab at external rotation, segue into a Milch, and then, in a nod to the OG, finish off with a Hippocratic maneuver!

I like the backwards ball cap - I'm calling this the "Bro technique." Let's not try this at the "port next time you're down there!

Found an ECG zebra... maybe.

Quick one today.

I wasn't sure about putting the case up, partly because there isn't a tidy follow-up and definite diagnosis yet. Also because I just talked about ECGs and PE, and this is material that is done better by Stephen Smith, or at Dr. S. Venkatesan's blog. Nonetheless.

I get ECGs tossed at me all day, checking for STEMI. A number of these are on folks under he age of 40, and I admit that my guard goes down a bit when I see the age. Nothing's impossible, but... Probably not on my shift.

So the tech comes up to me, hands me the 12-lead, and says "He passed out."

Huh. This looks different.

So, when you are looking at the ECG for cardiac causes of syncope, 4 entities you cnned to consider are long-QT syndrome, WPW, Brugada, and hypertrophic cardiomyopathy. Residents are good at describing the ECG appearance of the first 3, but are a little hazy on HCM.

Well, it looks a lot like the ECG above! I'll briefly review the manifestations of HCM on the ECG, boiling down a few of the references. Speaking of which, you may do as well to stop reading this post, and just download the great article by Kelly, Mattu, and Brady. You can download it here (pdf).

A few essential facts about HCM and the ECG:

• Most ECGs in patients with HCM will be abnormal.
• The ECG may be abnormal even if the echocardiogram (often taken to be the diagnostic standard) is normal.
• Signs of LVH are typical, including the high R-waves, and the concomitant ST-T wave depressions laterally.
• Q waves are often found in the inferior and lateral leads, erroneously suggesting old MI.

These Q waves are different from infarct-related Q's, however. The are deep and narrow, and have been described as "stiletto-like." Here's an example from the Kelly paper:

Unlike ischemic Q's, the HCM variety are generally under "one small box" in width, but may be fairly deep. Deep has been defined as 1/3 or 1/4 the height of the succeeding R wave (which my guy had), or at least 3 mm in depth in at least 2 leads (ditto).

So, did he have HCM? Hard to say at this point. The patient had an echo done, and was brought in for monitoring. The echo was limited, and no "obvious" abnormalities of chamber hypertrophy or outflow obstruction were found. If I hear more about his course, I'll share it.

Not just S1-Q3-T3: Pulmonary embolism and the ECG

When it comes to pulmonary embolism, there is more to the ECG than the presence or absence of S1-Q3-T3. Hard to believe, but true! Unfortunately, none of the other signs get quite as much press.

Not helping my case.

Let me give you the conclusion of this rant up front, in case you have better things to be doing.
When you are evaluating a patient for a possible PE, there are 4 things you should be looking for on the ECG:

1. Tachycardia
2. Incomplete or complete RBBB
3. T-wave inversions in V1 through V2, V3, or V4.
4. S1-Q3-T3

 Probably there are two reasons for this relative ignorance of the utility of the ECG in this setting. The first is a sense of nihilism. For example, how often have you received a "pimping" question from an attending along the lines of "What's the most common ECG finding in PE?" The attending-dependent answer is either tachycardia, or no ECG findings. Either answer may be true, if appropriately phrased and qualified, but really, you can't win.

Reprogram the scenario?

The implicit lesson is that the ECG will not be helpful in evaluating for PE.

A second reason, at least at Yale, is that we have been so well tutored on the use of electrocardiography to assist in the diagnosis of PE that the ECG seems quaint by comparison. After all, why would you care about indirect assessments, when you can just look at the heart?

Really, which of these technologies would most appeal to the Zune generation?

The essential study to know is the Daniel paper, from Chest in 2001. You should print it up and hit a coffee shop, beacause a quick glance at the abstract is not going to do it justice, so go ahead and download it here. Now, let me set the context, because studies on PE are nuts: the evolutions in technology and prevalence are just moving along so fast, it's really hard to keep up (Like with Zunes!).

The study used ECGs that were obtained on patients who were seen in the ED, and were suspected of having a PE. In current studies, that means a d-dimer was ordered, but in this study, back in the period 1997-1999, it meant patients who had a pulmonary angiogram. The rate of positive angiograms was 43%, showing that this was a group with a fairly high pretest probability of PE.

The authors developed an ECG scoring system, based on prior literature and case series, and wanted to see how well it could predict the diagnosis of PE. The nice part is that they used EM physicians (attendings and senior residents) as the readers, not cardiologists, giving it some real-world applicability.

The first important finding is that the ECG is not likely to be the best tool for diagnosing or ruling-out PE. Tachycardia was the most significant abnormality found on everybody, PE or no. A complete S1Q3T3 was found in only 7% more people with PE than without - not real helpful.

We already knew this, but I'm just going to stop there and reemphasize this results: You can't just look at any one sign on the ECG,  S1-Q3-T3 included. It won't help you.

They ran through the results a few different ways, and it's interesting to check out all the plots and bar graphs. The money graph, however, shows how calculating the total score can be used.

Put into English:

A score of ≥10 has a specificity of over 97% for the combined presence of a pulmonary embolism with severely elevated pulmonary artery pressures. 

That's a sick, sick patient. Of course, sensitivity stinks, less than 25%, but hey.

At least one case report has highlighted this use of the ECG - when you have a high Daniel score, and for various reasons you can't get imaging, it helps justify the empiric use of anticoagulants.

Well, this study doesn't really resemble what we do today, with al these pulmonary angigrams and such, so should the results inform our current practice? Marchick decided to run all the ECGs in Kline's PERC study through the Daniel score, to see how it could help.

Remember, to get into the PERC study, a patient just had to have some test for PE ordered - CT, V/Q, US, or a d-dimer. Not surprisingly, the rate of PE found in that cohort was below 6%. This is a far cry from the Daniel study, where 43% were positive!

Using a slightly modified Daniel Score, they found that the ROC curve for the score had a area of 0.61, consistent with the original study. More importantly, they looked at the individual elements:

Both S1-Q3-T3 and T-wave inversions from V1 to V4 have an LR+ of 3.7, which makes them fairly good, but not high enough to be decisive on their own. Fortunately, per their logistic regression...

... we learn that these two elements are independently predictive, and so we can use those, plus tachycardia, to suggest a PE. (Of course, this has to be in the right context. A patient with known pulmonary hypertension from other causes will show these same signs of RV strain).

So what? you say, holding your phased array probe over the patient, blue goop running down your wrist. If you can visualize RV dilitation, paradoxical septal motion, or perhaps even tricuspid regurgitation, what use is the ECG?

Echo: Useful in the evaluation of rigor mortis.

Some folks in the ED in Florence , Italy put down their espressos long enough to investigate the incremental value of the ECG and the echo in the prognosis of PE (not diagnosis - all the patients were known to have a PE).

It gets a little complicated for my little brain, but they essentially took a group of people who had been diagnosed with PE, and looked at 3 things:

• Which of the patients had signs of RV strain on the ECG, by Daniel criteria.
• Which of the patients had signs of RV dysfunction on echocardiography.
• Which of the patients had clinical deterioration or died.

So, when they boiled down the data, they found 2 important results. First, that ECG signs of RV strain are an independent predictor of clinical deterioration. It isn't a surrogate marker for echo data. Second, it appeared that signs of RV dysfunction by echo only predicts deterioration if there are already ECG signs of RV strain. 

The graph below show that echo evidence of RV dysfunction did not predict a bad prognosis unless there were coincident signs of RV strain (RBBB, T-wave inversions, etc.) on the ECG.

So, conclusion:

If you are looking at the ECG, and PE is in the differential, you need to look for all the possible indicators of right ventricular strain on the ECG. It gives you both diagnostic and prognostic information. No one will be pimping you on calculating the exact Daniel score, but you should be scanning for all the elements.