Ryan Ernst and I recently had a conundrum of a patient: she was chronically in A fib, and came to the ED after dialysis (she got a full run) because her heart rate was high. Like really high. Low 200s. The problem was that her blood pressure was really low. Like 70s/50s. So what do you do?

Shock her, right? She has an arrhythmia and is unstable, based on her BP. The thing was though that she was totally asymptomatic, had no complaints (not even palpitations) and is in no distress. We looked back in her records and saw that her blood pressure tends to run on the low side, although not typically that low.

So we decided to give her a little Cardizem (5mg) and see what happens. We were hoping that if we slowed down her rate, her BP would go up because her heart would have more time to fill. So we gave 5mg, and her rate came down a little. So we gave 5mg more. Then 5 mg more. Then started her on a drip. Her heart rate improved (was bouncing between 100-140ish), blood pressure came up marginally (and then would intermittently drop back down). We called CTO and MICU and let them deal with it. We were out of ideas.

So I’ve gone into the FOAM world to try to get some ideas about this problem. I found a good podcast from EMCrit (http://emcrit.org/podcasts/crashing-a-fib/) although I can just see the looks on the nurses faces when I ask them for phenylephrine, or ask to run a Cardizem drip at 2.5 mg/min and keep a very close eye on the patient.

One thing that’s particularly interesting from that podcast is that apparently, you can shock these patients, but if they’re chronic Afib patients, it’s usually not going to work. This was news to me. So Weingart recommends maybe trying some amiodarone, and if that doesn’t work, use some push-dose phenylephrine to get the BP up so that you can start them on a more aggressive Cardizem drip without tanking their pressure. I’d be curious what you all think of this strategy.

This also got me thinking about calcium channel blockers vs beta-blockers for regular old AF with RVR (in a non-hypotensive patient). There is an AWESOME blog called emlyceum (emlyceum.com) that is from Bellevue hospital and overseen by Dr Anand Swaminathan. All of their monthly posts are very evidence-based and provide links to all of their references. The put up a post a few years back on this very question of BBs vs CCBs, you can find the answer here: http://emlyceum.com/2014/01/17/medication-comparisons-answers/. I would highly encourage you all to check out this very good blog.

That’s it for now, please share your thoughts/experiences, that’s what makes this fun!

We have all been taught the two types of vertigo: peripheral and central. Peripheral is no big deal and you can send the patient home, and central requires hospital admission and typically work-up for a posterior circulation stroke or vertebrobasilar insufficiency, etc. We have also been taught, or led to believe, that history and physical examination will reliably help us to distinguish which of these two we are dealing with.

Classically, peripheral vertigo has a sudden onset, severe nausea and vomiting, bad ataxia, is positional, is associated with horizontal nystagmus, etc and central vertigo has a more insidious onset, the dizziness isn’t as bad, it tends not to be positional, the nausea and vomiting isn’t that bad, and you may see vertical nystagmus.

What you all need to be aware of is that while it’s a cute idea to think that we can reliably differentiate peripheral vs central vertigo by H+P, and these distinctions make for great board questions, it is NOT reliable and you should not use the criteria to definitely exclude a central cause for your patient’s vertigo.

Just the other day, I had a lady come in, in her 60s, relatively healthy, complaining of very sudden onset (while crossing the street) vertigo, nausea and vomiting. She had just been working in her garden and blamed the insecticides she was using. When I heard the story from the med student, I was hoping for my first organophosphate poisoning and was getting my atropine and 2-PAM ready, but unfortunately that did not pan out. We checked some labs, gave her some fluids and antivert and Zofran, with hopes of getting her better and possibly sending her home. She seemed like kind of a nervous nelly. My last step was to have the med student stand her up and have her walk. She failed miserably. She vomited just upon standing and felt she could not ambulate. So I admitted her, gave her an aspirin, and had neuro see her and do an MRI. Lo and behold, she had an acute right-sided cerebellar infarction.

This is by no means the first time I’ve had an older person with a posterior circulation stroke. Here are some tidbits I want you guys to remember:
-I haven’t seen a ton of them, but 100% of them had sudden onset of vertigo with pretty severe nausea/vomiting, despite those symptoms being classically relegated to the “peripheral vertigo” domain
-100% of them had totally normal head CTs, but proven cerebellar infarctions on MRI very shortly thereafter

Always walk your vertiginous patients before you even think about sending them home. If they can’t walk, you should probably think twice before you discharge them. Also know that in no way can you rely on your head CT to evaluate the posterior fossa. I’ve had patients with hemorrhagic posterior strokes with normal head CTs. Head CT does NOT visualize the posterior fossa very well, if at all. And please don’t rely on the traditional teachings of peripheral vs central vertigo. If it were that easy, someone would have devised a questionnaire, to be given in triage, with an Rx for antivert and discharge instructions to be given to all patients who qualify for “peripheral vertigo” on their vertigo questionnaire.

That’s it! As always, please comment with any of your thoughts, questions or experiences!

A recent guest at one of my weekend home BBQ’s was a friend of my brother’s who has a PhD in psychology who does  a lot of clinical research involving street drugs. She ended up getting a $1 million NIH grant so that she could buy a bunch of drugs and study some of their effects, and also to try and find antidotes. She literally pays addicts to come in to her lab, do some lines of coke, and be monitored for a couple hours. Very interesting stuff.

Besides learning that there may be someone out there who has a cooler job than me, I was also interested to hear her talk about marijuana usage. She particularly mentioned the cardiovascular effects of marijuana usage, including the profound tachycardia that it can cause acutely. I asked her if this was a common adverse effect, and she said that marijuana increases most people’s HR by at least 20-30 beats per minute, and casually said “everyone knows that”.

Well, I did not know that, so went to Google Scholar to investigate this more thoroughly. Sure enough, the cardiovascular effects of marijuana usage are pretty well-researched and studied. I found a nice overview article (that is also pretty short – BONUS!) that outlines some of these common cardiovascular changes that result from smoking the ganja. Here is the link: Marijuana as a trigger of cardiovascular events: speculation or scientific certainty?

Here’s a summary of the most important points:

-THC can definitely increase heart rate acutely, apparently by 20-100%! Apparently the maximal HR increase is seen within 15 min after peak THC plasma concentration and can last up to 3 hours!

-THC can decrease peripheral vascular resistance. As a result, “orthostatic hypotension has been frequently associated with marijuana use and both syncope and near-syncope can occur”.

-THC has a proarrhythmic effect, possibly catecholamine-mediated

There is a list of other cardiovascular effects, but these were the ones I found most interesting. If you think about it, if a patient came in tachycardic and syncopal, I would probably immediately start asking about DVT/PE risk factors, not whether they had just smoked a joint. Of course, anyone with tachycardia and syncope should be ruled-out for PE in some way, but I didn’t even realize the marijuana alone could cause these symptoms.

Given the extremely high marijuana usage rate in our practice, I thought it was worth sharing this information with those of you that also were not aware of these cardiovascular effects.

Steve Irving also sent me the chest x-ray seen below. Ignore the bullet in his chest, that’s old. This guy had a pneumothorax secondary to smoking marijuana. Maybe marijuana’s not as benign as I previously thought?

Hi guys

Before you skip reading this blog post because you think it’s gonna be boring, just give me a chance. I recently listened to a podcast on ERCast called “Mind The Gap: Anion Gap Acidosis”. A special thanks to Abdallah for encouraging me to listen to this. I have been aware of it’s existence for months but hadn’t listened to it because it sounded like snooze-ville to me.

Little did I know that it was actually interesting and had info I was not aware of! So here is a list of some of the interesting things that I learned, although I would encourage you all to take the 30 minutes to actually listen to the podcast, it’s worth it!

1. A serum calcium level can be a good surrogate marker for ethylene glycol poisoning. Many of you will ultimately end up practicing somewhere where it takes days for a toxic alcohol panel to come back, so you have to use your noggin to decide if someone may have a toxic alcohol poisoning. I never knew that you could use a serum calcium level (it will be markedly low, like 5 or 6) as possible evidence of ethylene glycol poisoning. (It is low because the calcium gets used up to make calcium oxalate crystals in the urine, remember those?)

2. If you think that your patient’s elevated anion gap is from AKA (alcoholic ketoacidosis), it should improve with fluids and glucose within 1-2 hours. If you recheck the lytes and there isn’t significant improvement in the anion gap, it’s probably not AKA and you need to think about other stuff (like possibly toxic alcohols).

3. If the patient has an anion gap and has an ethanol level > 100, it’s less likely that the patient’s elevated anion gap is due to a toxic alcohol because the ethanol would protect the patient from metabolizing the toxic alcohol. Remember that it is the metabolites (not the toxic alcohol itself) that are dangerous. The exception to this would be if the patient drank the toxic alcohol first, then the ethanol.

4. Interpret the osmolar gap carefully. A “normal” gap is -14 to +14. So lets say your patient normally has an osmolar gap of -10. They drink some methanol, and increase their gap by 20 points. Now their gap is +10. We wouldn’t think much of that, because it’s in the “normal” range. So just be careful, particularly if there is high clinical suspicion.

5. This is a very cool little tidbit involving the lactate level: ethylene glycol will cause a falsely elevated serum lactate level on the point of care lactate level, if it’s available. So if the POC lactate level is elevated but the serum level is normal, suspect ethylene glycol.

6. Patients with ethylene glycol poisoning will often have a bicarbonate level that is single digits.

So that’s what I learned from this single, 30 minute podcast. Tons of cool stuff. The reason it focused so much on toxic alcohols is because they are hard to diagnose. Most of the items in the MUDPILES mnemonic can be figured out easily with standard lab testing; the toxic alcohols are more difficult. They end the podcast with the advice to use fomepizole if in doubt.

Please leave comments!

So I heard about an incredible case from the overnight shift that I had to share with you all. First off, everyone should give Sharmin a big high five because she made the diagnosis, which is an incredible feat given that this patient had NO chest pain, but a HUGE dissection. You’ll have to ask her the details, but apparently the patient did have chest pain at some point prior to arrival, but it had resolved. The patient was also hypotensive. The lack of chest pain got me thinking about this case, and how common it is to have a dissection without chest pain.

I found this article with a nice table with the prevalence of different signs/symptoms (you can click on the table to enlarge it):

Features of aortic dissection

You will see that from this table, the prevalence of chest pain in this group of patients was 72.7%, so the majority of patients had CP. But that means that more than 27% did not have chest pain! This surprised me a lot.

Another interesting feature of this patient was her chest x-ray, which is presented below. You should note that the read by the radiologist was that the x-ray was essentially negative. The radiologist commented that the aorta was tortuous, but stated the mediastinum was within normal limits.

This underscores the importance of always looking at imaging yourself. Below is a list of x-ray findings that are possible in patients with aortic dissection:

-Widened mediastinum (present in 80%)
-Double aortic knob sign (present in 40% of patients)
-Diffuse enlargement of the aorta with poor definition or irregularity of the aortic contour
-Inward displacement of aortic wall calcification by more than 10 mm
-Tracheal displacement to the right
-Pleural effusion (more common on the left side; suggests leakage)
-Pericardial effusion
-Cardiac enlargement
-Displacement of a nasogastric tube
-Left apical opacity

I think that if you Monday-morning quarterback this x-ray, you could definitely argue that the mediastinum is a little wide and there is tracheal displacement to the right. The comment that the aorta was “tortuous” could presumably mean that there was “irregularity of the aortic contour”. By the way, you should know about these chest x-ray findings because I have seen a question on the in-service (or maybe on an in-service prep question) regarding what x-ray findings are indicative of aortic dissection.

Anyways, Sharmin was wise enough to order a CTA on this patient, and here are some pics of what she found:

Pretty impressive. The outcome of this patient remains to be seen; she was just admitted a few hours ago. We could also comment on the treatment of aortic dissection and the possible usage of D-dimer to screen for dissection, but I don’t want this post to be that long. If anyone wants to mention any of these things in the comments section, please do!!

Although the lumbar puncture is a cool procedure, and very satisfying when it goes as planned, it is time-consuming, possibly painful to the patient, requires discussion/consent that can take a fair amount of time, and requires CSF fluid analysis which can also take a lot of time. It also requires skill (and occasionally luck), which some have more than others. What this all boils down to is most emergency physicians hoping that there is a better, easier test than an LP when we are ruling-out subarachnoid hemorrhage (SAH) in our headache patients.

When I was a resident, I remember distinctly that there were widely varying practices among attendings. Some were fine with just getting a plain CT and stopping the work-up there; some wanted CT/CTA; others wanted the traditional CT followed by LP. I was given variable explanations for these practices, and was left wondering: who was right?

If you really want to listen to some good lectures about SAH in general and have this question (and many others) answered thoroughly, you owe it to yourself to listen to SMARTEM’s podcasts entitled “Subarachnoid Hemorrhage: A Rational Approach” from Dec 18, 2010 (1h 53min) and the newer “SAH: A Picture is Worth a Thousand LPs” from Nov 7, 2012 (2h 11min). If these seem too long for you, you can hop over to ERCast’s podcast entitled “The Subarachnoid Enigma” from May 8, 2015 (19 min).

Here’s the spoiler alert: CTA cannot replace LP. To be specific, we are talking about patients with a normal plain CT and a normal neurological examination. The problem with CTA is that it is very good at finding aneurysms > 3mm. Great, right? No! Because the issues are:
1. The CTA will NOT tell you if that aneurysm has bled at any point in time
2. Roughly 2.5% of people in this country have aneurysms, so it may be a completely incidental finding.

So who cares if you find an aneurysm incidentally, haven’t you still done the patient a huge favor? Not necessarily…You have now basically assured the patient that they will get an angiography (the real, invasive kind) and possibly a neurosurgical intervention. These are not benign procedures and have significant complications and fairly high complication rates.

So you need to do the LP. Still don’t believe me? Check out these resources:

-Life in the Fastlane has a nice general summary of headache assessment/management in the ED
Life in the Fastlane link

-There is a wonderful article in Academic Emergency Medicine called “What are the Unintended Consequences of Changing the Diagnostic Paradigm for Subarachnoid Hemorrhage After Brain Computed Tomography to Computed Tomographic Angiography in Place of Lumbar Puncture”. You can view the article in it’s entirety with this link: CTA in Place of LP article

I really encourage you to take a look at these things so that you can have an active discussion with your attendings while working-up these patients and so that you are knowledgeable about this very important topic.

Please share any questions/comments you may have!

As you all may be aware, there is a fair amount of controversy surrounding the use of tPA in acute ischemic stroke. This becomes even more apparent when you talk about extending the “stroke window” to 4.5 hours. Rather than give you my personal opinion on this topic, I want to give you all a list of resources so that you can be well-informed and make your own decision. To do this properly will take some time on your part, but I promise you that this issue is not going away anytime soon. You need to fully understand this medicine so that if you give it to a patient and they die of an intracranial hemorrhage, you still feel that you did what was best for that patient at that time. Below are some recommended things to check out, including stuff that has been released in the past month.

1. Podcasts. There are several extremely high quality podcasts on the topic. If you want the quicker one (55 minutes), check out “Acute Ischemic Stroke” from the Oct 14, 2013 podcast of ERCast. Very good, but an overview. If you really really want all of the details and want to fully understand this topic, check out the June 28, 2012 episode of SMARTEM entitled “Thrombolytics for Acute Stroke” (2h, 35 min) and the August 12, 2013 update entitled “Thrombolytics for Stroke: Update” (1h, 23 min). I have listened to both of these twice because the information is so important, and they make the discussions fun.

2. You can always read the original articles and interpret the findings for yourself. The show notes for the above podcasts list the articles. Here is a link to the classic NEJM articles (about the NINDS studies): NEJM article
Of all of the tPA studies to know, NINDS may be the most important because it was the basis for the recommendations to give tPA to our patients. You should know about this study, and it is very helpful to look at the “Letters to the Editor” (you can click directly to these from the article) and see why a number of smart people didn’t like the study. They actually had to do 2 NINDS studies because NINDS-1 (looking at 24 hour outcomes) did not show any benefit to tPA. For those of you thinking, “I gave a patient tPA and they were much better 2 hours later”, it’s probably because you tPA’ed a TIA. Very interesting stuff.

3. Check out the March, 2015 edition of ACEP Now (it’s that monthly newsletter that we all get and occasionally read). Here is the link. Essentially, the clinical guidelines recommending tPA are changing. They used to be level A recommendations and there was such outrage that they are changing to level B. Below is a screenshot from the cover of the newsletter.

4. This is not a recommendation of something to read, but I wanted to share with you an item I received in the mail within the past month. It is pictured below and appears to be an update on stroke management. Look at the company that sponsored it (I zoomed in on it in the second picture). Guess what drug Genentech manufactures? Thought this was interesting as Genentech has their hands in a lot of the “research” that is being done on tPA and I felt this was particularly egregious to send something that looks like it might be legit (and you get CME for reading the article!) that is full of biased tables and charts (I can show it to anyone that’s interested).

Ok, that’s it for now. Just wanted you all to be aware of this current debate and to form an opinion on the matter. Ask your attendings how they feel about it. You’ll get wildly different answers from different attendings (trust me, I’ve already asked), and people tend to feel pretty strongly one way or another because the topic is so polarizing. Please post your thoughts and comments below!! And no, I’m not completely anti-tPA, I just personally don’t feel that we have narrowed down which patients will benefit and which won’t, and to give it to everyone indiscriminately seems not right to me…

Last week, I had a patient who came from dialysis with bleeding from his AV graft. He had completed his entire dialysis session without any problems, and when they removed the needle from his graft, he started having bleeding. Pressure was applied, but to no avail. By the time he got to us, intermittent pressure had been applied for an hour without stoppage of the bleeding. I was going through some different treatment options, and thought it would make a good blog post. For clarification, this guy was having definite arterial bleeding. Not shooting-across-the-room type of arterial, but pulsatile with a significant amount of blood loss.

What I ended up doing is placing two figure of eight stitches. Here is a very cool YouTube showing this procedure: https://www.youtube.com/watch?v=toFiGSfesZk

You should definitely know how to do this. I also talked with the senior vascular surgery resident. He said he likes to take a piece of gelfoam, place it over the spot that’s bleeding, hold gentle pressure for 10 minutes (not hard pressure; that could occlude the graft and cause it to clot off = bad). He assured me that this works even for arterial bleeding.

A quick search yielded these recommendations from ACEP: https://www.acep.org/Clinical—Practice-Management/Focus-On–Dialysis-Access-Emergencies/
Note that the authors are former SGH residents and Dr Barton! Very cool!

If the patient is not having arterial bleeding and is more just oozing, I like DDAVP. You also have to consider protamine if the patient is coming from dialysis because they do get heparin during dialysis.

Take home points: consider throwing in some figure-of-eight sutures, using gelfoam, or possibly using medication (DDAVP, protamine) to stop the bleeding from an AV graft/fistula.

What other bleeding problem is DDAVP used in? How does it work? Why does it help dialysis patients?