Monthly Archives: November 2015

Humanity

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This is a commentary on this article by a resident reflecting on life, trauma, and death. The  resident’s self-reflection is a nice read and something with which we can all identify. But the “meta-reflection,” if you will, is something we do not usually get to see in our EM journals. We read one or two essays in each Annals, sometimes in Academic EM and in JEM. I tend to read these first or tear them out and hold them until I can read in a quiet room and really concentrate on them. And I do my own reflecting on the themes and ideas presented by that person.

The commentary article describes the difficulty in a self-analyzing essay. The schizophrenia and detachment involved in presenting your own thoughts in this way. Dr Ratzan reviews some of the (sadly few) accomplished physician writers and their themes. William Carlos Williams was a poet/writer and physician. Richard Selzer, a retired Yale surgeon, is still living and I hope still writing. His books are so rich and he is so talented a writer that I can hardly read more than 20 pages at a time. Brilliant physician writers are rare but essential to the humanity of our profession.

And emergency medicine in particular, with its intensity and ?necessary detachment, might need this humanity more than any other specialty. I recommend we all read something either in the medical humanities, or something seemingly unrelated to medicine. You might think the literature or the book of humor or the young adult futuristic death competition book is non-medical. But connecting, or reconnecting, with that part of yourself that is separate from the ED will make you a better doctor and healer.

It can become trite to say feelings are important, we need to have empathy, there is a human side to this job of ours, etc. And it is a difficult jump from reading a feel-good essay to the next day walking into the room of a patient with fibromyalgia and trying to channel that empathy you were just reading about. But trust me, if you make an effort to do this you will appreciate your patients. Good advice I read from a Brazilian shaman: “remember that the world does not revolve around you.” you have to really think about that to understand. Try to picture the world through literally through other people’s eyes, makes yourself and your troubles seem smaller.

The patient you are seeing in the ER is likely having the worst day of his month or year or even life. Try not to forget that. Happy Thanksgiving.

The EKG in Palpitations

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Late 20s female w CC of chest discomfort and palpitations, n/v x 1 days. No recent illness, no fever/chills/diarrhea. Says the episodes come on abruptly and last less than a minute. No h/o early cardiac disease or early death in family. Says she feels short of breath with the episodes and her chest feels tight. Denies tunnel vision. Denies syncope but feels like she could pass out. ROS o/w positive for anxiety (grad student). Denies T/ETOH/D. Social history o/w irrelevant. No allergies. Only medicine is OCP. Exam is unremarkable (heart normal, lungs clear, appears well).

What would you order on this young patient with this complaint? How would you document it?

I have recently seen a few charts in this and similar patient presentations that gave me pause. I’ve seen workups from EKG alone to the full cardiac rule-out and everything in between. The only true unifying theme, and I think rightly, the most important test is the EKG (aside from a pregnancy test).

And most of the charts have a documented EKG. Ok. No problem there. Below is an example of a chart documented on a <30yoF patient with Palpitations…

 

Normal_ECG

“NSR, Rate 85, Normal P waves. No S/T wave changes. Normal QTc. No ischemia. No EKG for comparison. “

 

The problem with this? Aside from a few parts, it is mostly irrelevant to the life or limb threatening abnormalities that we are looking for in the EKG. Sure, it will bill just fine, but I worry that there a few among us who aren’t SPECIFICALLY looking at the EKG in the palpitations patient for common causes of palpitations. I mean, really, how many of us see MIs present as palpitations?

 

So what should you look for in an EKG in a palpitations patient?

  1. Rate (tachy or brady or no?)
  2. Blocks
  3. HOCM
  4. Brugada
  5. AVRD
  6. Prolonged QT (cong. QT) or Short QT (why?—AVRD)
  7. WPW
  8. Ischemia

 

Now lets talk about the EKG abnormalities found in each:

HOCM—About 90% of HOCM pts have an abnormal EKG. Remember, these are often young folks, so their ekg should be pristine. The etiology is a hypertrophic septum, so characteristic LVH is seen (V4R wave is “off the chart”), as well as deep, narrow q waves laterally. Occasionally flipped, broad T-waves are seen. There is also an apical variant that shows GIANT TWI in septal and lateral leads… you’ll know it if you see it, it looks grossly abnormal. But HOCM itself can be much more subtle. Look for Q waves and LVH then listen to their heart and refer to cardiology for an echo. Both of the below are pretty obvious, the second one is the GIANT TWI i was talking about. Not a lot of things do that.

time 4 hours HR 84

HypertrophiccardiomyopathyapicalvariantYamaguchisSyndrome

Brugada— 50% familial, most present >20yo but can be seen at birth. In brugada, you’re looking at leads V1-3, looking for a Right bundle branch block and either “coved” (st elevations with long, flat ST-segment that looks like a ski-slalom) or the “saddle type” (which is way less common and looks a lot like, well, a saddle. But remember there is STE there too which makes a side of the saddle, then the T-wave makes the other side of the saddle. This sometimes looks like a STEMI, except in a patient without chest pain and then you notice the saddle shaped concave ST segment and the CC and family history and you can smile because you didn’t activate the cath lab. Also, these patients can have EKGs that show brugada pattern SOMETIMES and not other times. Look for the ski-slope and the saddle. Hop aboard this saddle and you’re going to need a defibrillator, as anti-arrythmics don’t change mortality much….

14_minutes_QRSd_146ms_p_2_Amps_bicarb_axis_167

255v62n11-13145482fig1

This image says there are 3 types. OK, well, that’s true and all but seriously, it’s still a saddle, so you shouldn’t be led astray.

AVRD- What the what? AVRD stands for arrythmogenic right ventricular dysplasia, and basically their RV gets filled up with fat and cartilage during development. This is not so good. These folks may have exertional chest pain (it’s a cardiomyopathy). And, because it’s a structural heart disease, most of them will have EKG abnormalities (~90%). The most specific finding is an EPSILON wave, which is a little puny looking bump after the QRS that looks like a little P wave but is out of place and behind EVERY QRS. These are hard to catch, so you HAVE TO LOOK FOR IT IN PARTICULAR! Also, remember, not every Osborne wave is AVRD (is the patient hypothermic?) Occasionally this will make the QT interval short, but it isn’t reliable. Other, less specific findings are TWI in V1-3 that looks like a juvenile pattern… but remember juvenile pattern should go away when the patient becomes less juvenile. So if they have TWI in percordial leads an they are >20 and have palpitations or syncope… PANIC. No, but really, they probably have AVRD. And the syncope was probably VTACH. But they’re good now, right? Give them a defibrillator too.

avrd_figureone-2

 

Oh, crap. That’s what happens when you send the patient home without looking for AVRD.

 

ARVC

Congenital Prolonged QT-– Ok, so a bit of an update to our usual shortcut “half the R-R rule,” in Academic Emergency Medicine in October 2015, some folks published a retrospective review of some cases of EKGs with prolonged QT and non prolonged QT, and found that our quick half the RR interval thing is about 88% sensitive (r/o prolongation) but only 53% specific. Which ain’t terrible, but its also not super good (12% aren’t ruled out). Of course, what the study failed to highlight but is written and useful is that the ½ RR rule is 100% sensitive (in this study) if the HR was >60. So my take is, if they are brady, calculate it yourself, and if not, 1/2RR is good to go. Which is what I think most of us do anyway. Three cheers for studies confirming our guesses!

Screen Shot 2015-11-08 at 5.44.26 PM
WPW—Not much to say here. You know this. And you damn well should be documenting it. That PR interval is short because your patient is dying for you to find his delta wave.

Wpw

ACS– Well, this is what we do.

Blocks- P before every QRS, QRS after every P. Intervals.

 

So… how should you be documenting these EKGs? With the same attention to the life and limb threatening abnormalities you are looking for on your history (early family death) and exam (murmur?). I can’t say what is right or not, but below is how I would document that EKG on our patient from earlier (NSR, rate 85, No STE/D, No TWI, no definite EKG evidence of WPW/AVRD/CongQT/blocks/HOCM).

Cheers.

 

Images:

https://meds.queensu.ca/central/assets/modules/ECG/Normal_ECG.bmp

http://hqmeded-ecg.blogspot.com/2014/06/history-of-hypertrophic-cardiomyopathy.html

http://www.doctorshangout.com/photo/hypertrophic-cardiomyopathy-apical-variant-yamaguchi-s-syndrome

http://hqmeded-ecg.blogspot.com/2013/05/brugada-pattern-induced-by-tricyclic.html

http://www.revespcardiol.org/imatges/255/255v62n11/grande/255v62n11-13145482fig1.jpg

http://www.geneticheartdisease.org/jpegs/avrd_figureone.jpg

http://www.heartpearls.com/wp-content/uploads/2009/07/ARVC.jpg

http://www.crkirk.com/thumbnail/arrhythmias/images/svt/ECG_WPW.htm

Another abdominal pain

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I had a patient in her 30s that presented with 1 day hx of N/V and diffuse abdominal pain that was most severe in her epigastric and LUQ and radiated to her back.  She had PO intolerance since the pain started the night before. Past medical hx was significant for R nephrectomy that she states is because her “kidney wasn’t working right”. Pt says that this pain feels just like the pain she had from that kidney.

PE: VSS, afebrile. She is curled in the fetal position and yells anywhere you touch on her abdomen but states that the worst pain is when I press her epigastrum and LUQ. She has a large RUQ scar from her nephrectomy. No CVA ttp, negative murphy sign.

At this time my differential included pancreatitis vs PUD vs gastritis vs pyelonephritis
Labs come back with lipase wnl, no WBC, UA with a lot of epithelial cells and a few WBC. Acute abdominal series xray is wnl

I reassess patient after dilaudid and zofran and she states nausea has resolved but still has severe epigastric/LUQ pain. On reexamination the rest of the abdomen is nontender. The amount of pain she is experiencing in her epigastrum/LUQ concerns me and its not pancreatitis based on the lipase so I order a CT abd/pelvis and I put in the ordering comments “diffuse abdominal pain most severe in epigastric and LUQ”.

The radiologist walks over to the department to tell me that the patient has appendicitis and her appendix which is thickened and with fat stranding is in the mid right abdomen instead of RLQ hence the atypical location of her pain. My assumption is that the reason her appendix is so high is from scar tissue secondary to her transabdominal nephrectomy.

I post this to remind everyone that while the RLQ is the most specific place to have pain from appendicitis, the pain can be anywhere (previous abdominal surgery (in this case), retrocecal/pregnancy, etc).

Approach to PE

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Hey all,
I got the privilege of going to ACEP last week in Boston. When I got the schedule one of the lectures that stood out to be was a PE lecture by Jeffrey Kline. Some of you may recognize the name but if not, he is an attending at IU with a special interest in thromboembolism. He is very active on twitter at @klinelab and wrote the Thromboembolism chapter in Tintinalli’s. After talking about PE last month and specifically approach to PE in the pregnant patient, I thought a summary of the key points would make for a worthwhile post.

The first question in the discussion of VTE should be ‘who actually needs to be tested?’ If someone comes in complaining of recent chest pain or dyspnea, PE needs to be included in the differential. If they are not complaining of those recently and have normal vitals (at all times) then you don’t need to go chasing down a clot that isn’t there. If the patient does complain of those then some sort of documentation is required to show you considered a PE. Even stating ‘I think PE is unlikely because of X, Y and Z’ would likely be enough. Now if your pretest probability is anything other than very low, some combination of wells, perc, Geneva should be applied. I like the following algorithm which I think Kline discussed on EMRap towards the end of last year.
algo

Following that algorithm helps cut down on the number of ct scans you’ll order, cuts down your false-positives, radiation exposure, and contrast induced nephropathy without increasing the number of significant PE’s that you miss.

As far as the pregnant patient, I think everyone knows to start with the lower extremity ultrasounds in hopes of an answer that would let you initiate treatment. However, when that is inevitably negative, there is also an algorithm for that scenario that incorporates a trimester adjusted d dimer.

algopreg

The other main takeaway from this talk was the disposition change on some of the low risk patients. Dr. Kline said he has sent about 70 patients home from the ED after being diagnosed with PE. To stratify who falls into low risk, you can apply the sPESI or HESTIA score as well as who is at low risk of bleeding.

–Simplified PESI-if any +, pt is NOT low risk:
age greater than 80
history of cancer
history of chronic cardiopulmonary disease
pulse greater than 100
BP less than 100
O2 sat less than 90

–Hestia-pt CAN BE considered low risk if
BP greater than 100
No thrombolysis needed
No active bleeding
02 sats greater than 90
Not already anticoagulated
No other medical or social reason for admission
Cr clearance greater than 30
not pregnant, no severe liver disease

For these people they’ll initiate rivaroxaban or apixaban in the ED and send them home with a prescription. The only failures they’ve experienced are people who returned requiring additional pain management. Has anyone done this or considered it? The majority of our patient population would not satisfy these requirements or, frankly, be reliable enough to consider outpatient management, but what about people working in the community with a different population?

Lastly, we all know to look for S1Q3T3 on the ekg to raise suspicion for PE but the odds ratio is only 2.06. Inverted T’s in V2 and V3 have odds ratios of 6.94 and 7.07 respectively, and are the most SPECIFIC ekg finding in pulmonary embolism

Better to be lucky than good

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I was called to a code in the ICU.  I roll into the room, 38yo IVDA hx, admitted for sepsis, septic emboli, and ARDS.   Stable vital signs 10 minutes previously, now in PEA arrest.  Already tubed and had a triple lumen in the IJ.   Not a whole lot for me to add for immediate stabilization with a secure airway and access.   Already had epi x1.  Accucheck was 149 (never, never forget this in a code).

So I immediately get to go to the second phase and start thinking reversible causes.  With that hx, all sorts of interesting diagnoses on the playing field.  The one major thing I notice was the patient was extremely cyanotic from the upper chest on up.   CBC and BMP from a few hours ago essentially unremarkable aside from a white count of 26.  Coags normal.  Actually starting to kick around the idea of empirically thrombolyzing this dude.  All of a sudden, quick run of v-fib, zap him with 200 and voila! we have a pulse.  I order a new rainbow of labs, cxr, call his pulmonologist to recite my efforts,  and strut back down stairs with a little gangster lean feeling pretty good.

I sit down, take a deep breath, and head to see the next patient.  And BOOM!  Code alarm goes off once again.  Head back into the room, next verse same as the first.  Guy suddenly went PEA arrest again, CPR was already in progress.  No labs back.  I have them pull up the CXR.

IMG_3103

Well sh*t, I swear I listened to him during the first code.  Bilateral breath sounds (course, but there).   I listen again, knowing there is a big pneumo, still can hear.  Obvious tracheal deviation on the CXR, but time to get moving.   So I ask for an angiocath and a chest tube set up.  Deer in headlights, no one moves.  Someone finally scurries off to find a pleurovac and tube.

Still waiting for an angiocath, they hand me something that looks like something I’d LP a 10 day old with, not gonna cut it.  Finally they roll in with this kit that looked like they pulled off a dusty shelf.  Has what looks like a 8 inch spinal needle with a pigail catheter already attached to it.  That’s it.  nothing else in the kit besides and adaptor to attach to the pleuravac.  Don’t have a lot of time to search for anything else so I went with it.  Was actually really slick- put the needle into the chest cavity, pulled out the inner cannula, heard the hiss and fed the pigtail.  That’s it, working chest tube in place in about the same time it would take to do a needle decompression.

IMG_3105

Immediate return of pulse and stable blood pressure.   Thank god.  That would have been a totally reversible cause of death in a young patient.  If I hadn’t ordered or remembered to check that x-ray, would have been on my shoulders.

I post this for a couple of reasons.

#1 Don’t get too cute in your codes.  Start with the basics and build from there.  I was too busy thinking about lytics etc, and had an easily reversible cause right in front of me.  Don’t forget your DOPES mnemonic for ventilated patients.

D- dislodgement, check your tubes, end tidal or even preferably direct visualization.  Especially in a patient getting CPR.

O- obstruction, always suction, mucous plugging is an easy removal.

P- Pneumo, already talked this through.

E- Equipment, I recommend always pulling your codes off the vent and bagging through the ET tube to take this one off the radar.

S- stacked breaths.  Too much PEEP or high respiratory rates without adequate expiration time can cause air trapping and decreased venous return.  Once you pull someone off the vent and bag.  Take a second and manually press the chest wall down.  Can fix the problem immediately and you look like a total ninja if it works.

2015 ACLS GUIDELINES

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The new 2015 ACLS guidelines were published this month!  I love new guidelines!  I’ve highlighted the important drug stuff (you guys are on your own for the rest).

Vasopressin: REMOVED FROM ALGORITHM: This was no surprise to me as vasopressin has never been shown to offer any advantage over epinephrine in studies to date.

“Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest (Class IIb, LOE B-R)”

“Vasopressin in combination with epinephrine offers no advantage as a substitute for standard-dose epinephrine in cardiac arrest (Class IIb, LOE B-R)”

Steroids: I’ve been skeptical of the use of steroids in cardiac arrest since 2009 inhospital cardiac arrest trial (steroids were combined with a vasopressor bundle or cocktail of epi and vasopressin).  Will need much more convincing data before I’ll recommend routine use- and that is exactly what our guidelines endorse as well.  Because: no one in the ICU dies before receiving a course of steroids.  The pre-hospital use of steroids is pretty clear: no benefit.

“In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post-arrest hydrocortisone as described by Mentzelopoulos et al may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy (Class IIb, LOE C-LD)”

“For patients with OHCA, use of steroids during CPR is of uncertain benefit (Class IIb, LOE C-LD)”

Epinephrine: Nothing groundbreaking here.  A few trials did demonstrate ROSC advantage with high-dose epi over standard dose; however, no improvement in survival to discharge (emphasis on good neurologic recover) over standard dose.  There is much concern with adverse effects of higher dose epi in the post-arrest period which may negate potential advantages during intra-arrest period.

“Standard-dose epinephrine (1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest (Class IIb, LOE B-R)”

“High-dose epinephrine is not recommended for routine use in cardiac arrest (Class III: No Benefit, LOE B-R)”

Antiarrhythmics: Really no changes.  Emphasized use of amiodarone over lidocaine (which is not new).

“Amiodarone may be considered for VF/pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B-R)”

“Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD)”

“The routine use of magnesium for VF/pVT is not recommended in adult patients (Class III: No Benefit, LOE B-R)”

Circulation 2015:132:S444-64