Brugada Syndrome

This 33 y/o male who came c/o palpitation episodes for very long time and more recent near syncopal episodes has Brugada syndrome. This, my friends, is VERY important diagnosis to make in the ED. Many, and by that I mean a lot, of ED docs and even cardiologist don't recognize the Brugada pattern. That is a sad, b/c we are in the business of saving lives and not making this diagnosis is a missed opportunity to save one and bad for business.

First, a little bit of history. Brugada is a relatively new electrocardiographic diagnosis considering that electrocardiography has been in use for almost 100 years, Brugada was discovered in the late 80's. The Brugada brothers (they are 9 super smart cardiologist) collected case series of young patients, mostly men and many of Asian origen, who had sudden cardiac death. Looking back in the available histories, these patients often complained of palpitations, dizzy spells, syncope or near syncope episodes and some had family history of unexplained deaths in young relatives. For those who had EKG's in files the pattern of down-slopping ST segment in V1-V3 with a complete or incomplete RBBB pattern was a constant finding. As technology advanced and genetic testing became more sophisticated, different gene mutations of the potassium channels were identified that predispose patients to fatal arrhythmias mainly polymorphic VT, VT/VF. Often times they self terminate and the only history we get is that of palpitations, syncope or near syncope, but in some cases sudden cardiac death is the presenting symptom of Brugada.

OK, enough of that... now let's see the EKG of this patient I saw few weeks ago. Note the STE in V1-V2. This is not the STE of ischemia, early repolarization or pericarditis, this is a down-slopping STE. This can have some small variations in the shape depending of what mutation is present, but the key point is that you are not supposed to have that STE pattern. Often it is associated with long QT, which is another important genetic mutation on it self with risk of Torsades de Points, and both can be seen in the same patient. The QT in this case in 454, which is in the borderline of prolonged.

Brugada is classified in different types, depending of the morphology and the genetics. But in all types, the down-slopping STE is the key to make the diagnosis. If it looks like a saddle or not is irrelevant, the key here is to identify Brugada. Look at the 3 types below, now close your eyes and make a mental picture for your long term memory. (I try that sometimes and occasionally it works :)

Another key feature of Brugada that you must not forget is about treatment. That is very easy b/c there is only one. The only treatment proven to decrease mortality is an intracardiac defibrillator. Anti-arrhythmics don't work, beta-blockers don't work, calcium blockers don't work, magnesium doesn't work, gummy bears don't work. That's why it is important we make this diagnosis and refer to an electrophysiologist pronto, so these patients can get their ICD and survive.

Now, this is another case I had few years ago. This guy had been seen in different ED's, seen by cardiologist, diagnosed with anxiety and let loose.

Again, note the down-slopping STE in V1-2. On the side, this guy also have a PVC, which may suggest some ventricular irritability as well. When I told this guy about the dx and tx, he asked me - Why no one told me about this? I have been seeing doctors for years! - He went to Germany to have his ICD and now has a normal life.

Key points

1.- Remember Brugada in every patient with history of palpitations, syncope, near syncope or family h/o unexplained deaths.
2.- Recognize the down-slopping STE in V1-3 with complete or incomplete RBBB pattern. That is the landmark of Brugada.
3.- The only treatment is an ICD. These patients need referral to an electrophysiologist, pronto!
4.- Gummy bears are good but not for Brugada.

Now, if you are really into EKG's, you may want to read more about this topic. Here is a complete review on Brugada from the cardiology literature. Maybe a bit too much, but interesting reading nevertheless.

http://content.onlinejacc.org/article.aspx?articleid=1125533

The Angry Patient

The main reason of me writing this blog is to share clinical information and comment about emergency medicine related topics; however, from time to time I get a little philosophical or find other topics indirectly related to the practice of medicine. This post is in the latter category. The interaction with an angry patient is that kind of encounter that can sour your entire day, mess up with your judgment and ruin your mood. In the ED we have quite a few of those on daily basis. Over the years, I have developed my own way to deal with this type of situations, but my method is not nearly as good as the one on this video. This dude brakes it down so well, that I am even looking forward to use this new skill during my next angry bird encounter (you play angry birds too, don't you?).

Here is the protocol: http://thehappymd.web13.hubspot.com/Portals/263814/Docoments/universalupsetpersonprotocol.pdf

Asymptomatic Hypertension in the ED. What Should We Do?

Patient in his 50's shows up to the ED b/c his high blood pressure. He has no other complains, his wife made him come in (you know how it is). He gets an EKG in triage (protocol says you get one for showing up) and it has some mild LVH, but no acute changes. You do a physical exam and there is nothing besides the smell of bean burritos with lots of garlic. What do you do...? Do you screen for organ damage (EKG, UA, Creatinine, CXR)? Do you just begin treatment? Do you screen and treat depending on what you find? Do you advice him to continue checking his BP twice a day and follow up with his doctor this week? Or do you recommend him to stop eating Mexican food and eat tofu instead?

Asymptomatic hypertension is so common and the pressure to treat a high blood pressure is very high, this is a real pain in my existence. The nurses frequently ask for "something" to treat the BP, even when the patient has no complains. And how you like this one? "The nurses upstairs will not take the patient unless the BP is less than whatever (insert your favorite number here)", even though the patient has had poorly controlled HTN for the last 200 years. At that point I have two options, give in and write the order for something (insert your favorite fast acting anti-hypertensive) and risk overshooting causing an unsafe drop in the BP or just ignore it, let the team upstairs deal with it and make the nursing staff believe that I am an uncaring physician.

Fortunately in May of this year, ACEP published an update on their 2006 clinical policy on asymptomatic high BP in the ED. They did a pretty extensive review of the literature on the topic and provide good guidelines in this common dilemma. It is important to note, these guidelines do not apply for patients with high BP and signs/symptoms of target organ dysfunction, the so called hypertensive emergency (stroke, acute myocardial ischemia, pulmonary edema, encephalopathy), pregnant patients, ESRD or trauma. I know, it sounds obvious, but just in case.

I will now summarize with 3 key points of this document.

Definition of markedly elevated BP is in agreement with the JNC7 classification of stage 2 hypertension, which is SBP > 160 or DBP > 100.

Screening. In the ED, patients with asymptomatic HTN, routine screening for acute target organ injury (eg, creatinine, UA, EKG, CXR) is not required. However, in selected population (eg, poor follow up) screening with serum creatinine my identify kidney injury and affect disposition. Evidence level C.

ED treatment. In patients with asymptomatic markedly elevated BP, routine ED medical intervention is not required. These patients should be referred for outpatient follow up. But in selected groups (eg, poor follow up), the emergency physcian may treat and/or initiate therapy for long term control. Evidence level C.

Furthermore, this document cites evidence that up to 32% of hypertensive patients have reduction in their SBP of > 20 mmHg and DBP > 10 mmHg after 30 minutes of rest, and that acute lowering of the BP does not improve short term outcomes and it may actually  be detrimental. "It is generally accepted that the rapid lowering of markedly elevated blood pressure in the asymptomatic patient has the potential to do harm".

So... what should we do with the patient above? Well, that may depend of how "labby" you feel that day or how busy the ED is. But this guidelines should be enough to give you a point of reference and do what is best for your patients without clogging your department.

And for those who want to dive deeper into this guideline business, here is the reference for your reading pleasure.

http://www.annemergmed.com/article/S0196-0644%2813%2900445-9/fulltext

Share this information with your colleagues, it may actually reach the people who make protocol decisions! 

Antibiotics to Prevent Burn Infection - Systematic Review

This is very interesting... For years I was taught, to smear the "white cool mayo" on burns to prevent infection. Now, I am not so sure I should continue doing that. Maybe applying Vaseline gauze is better (and cheaper) to protect the wound and with less risk of infection compared with the expensive "Silvadene". The same may apply systemic abxs. I guess everything goes back to the basics of good wound care.

http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008738.pub2/abstract;jsessionid=29FCB5487AAB811548AF3EDF1CF2E681.d03t02

Here are the critical findings

-  There was a statistically significant increase in burn wound infection associated with silver sulfadiazine compared with dressings/skin substitute (OR = 1.87; 95% CI: 1.09 to 3.19, I² = 0%). These trials were at high, or unclear, risk of bias. Silver sulfadiazine was also associated with significantly longer length of hospital stay compared with dressings/skin substitute (MD = 2.11 days; 95% CI: 1.93 to 2.28).

- Systemic antibiotics (trimethoprim-sulfamethoxazole) were associated with a significant reduction in pneumonia (only one trial, 40 participants) (RR = 0.18; 95% CI: 0.05 to 0.72) but not sepsis (two trials 59 participants) (RR = 0.43; 95% CI: 0.12 to 1.61).

- Perioperative systemic antibiotic prophylaxis had no effect on any of the outcomes of this review.

- Selective decontamination of the digestive tract with non-absorbable antibiotics had no significant effect on rates of all types of infection (2 trials, 140 participants). Moreover, there was a statistically significant increase in rates of MRSA associated with use of non-absorbable antibiotics plus cefotaxime compared with placebo (RR = 2.22; 95% CI: 1.21 to 4.07).

- There was no evidence of a difference in mortality or rates of sepsis with local airway antibiotic prophylaxis compared with placebo (only one trial, 30 participants).

Azithromycin's Black Box Warning - Shouldn't be Yellow?

In May of 2012 the NEMJ published an article about the cardiac risks of Azithromycin. This fake science was the base for recent decision of the FDA to issue a black box warning, which in my opinion was an overboard and wrong move. Last year I replied with this editorial, which I admit, it was a little harsh with a touch of my usual sarcasm, that's probably why it didn't get published. Nevertheless, I just want to add it to my blog for those who want read and think outside this black box (warning).

First, read it from the NEJM site:

http://www.nejm.org/doi/full/10.1056/NEJMoa1003833?query=emergency-medicine

According to the authors, it seems like you are almost 2.5 times more likely to die a cardiovascular death after a course of "Azithro" than you are after taking 7 days of Amoxil, and almost 3 times compared to no antibiotics at all. Which means that even amoxicillin has a hazard ratio of 0.5 compared to not taking any antibiotics. However... Let's put this in perspective, shall we?  Using the numbers provided in the result section, you need to prescribe 1,000,000 Z-packs to kill 47 patients with low cardiovascular risk and 245 with high cardiovascular risk. That means that even in the worse case scenario, the number needed to kill by one course of azithromycin is 1 per 4081 compared with 1 in 10,202 of amoxicillin. Hmmm... Do you want a more ridiculous number? - OK. Assuming that you prescribe Azithromycin once a day every day of the year; you need to practice for 11 years, non-stop and with no days off to kill one patient with high cardiovascular risk and 58 years for the low cardiovascular risk patients. Amazing, isn't? - To me this doesn't sound too bad when compared with the 27% mortality rate of sepsis with severe pneumonia or with other therapies we use, like warfarin that clearly has a higher risk of harm associated with it. What I would like to see is more details about the high risk patients. As statisticians say "The devil is in the details". In the first place, we don't give antibiotics to healthy people (so I hope), and using healthy patients as denominator just doesn't seem right. Then, there is the fact that Azithro is considered a "stronger" antibiotic compared to amoxi being a better choice for sicker patients. And why is it that Azithromycin is in the guidelines for the treatment of pneumonia and not amoxicillin? Was the choice of Azithromycin a marker or more severe disease and therefore prescribed to sicker patients who had more risk of death regardless of the antibiotic choice? - I don't know. This article doesn't answer that.

There is no question that antibiotics (and for that matter, any medication) will hurt some patients, that is just reality. Some will have minor problems and some others will even die as direct consequence of the drug. About 10 years ago my cardiology professor and I wrote an editorial about several types of medications and the risk of CV death by long QT syndrome (Headache. 2003 Jul-Aug;43(7):809-10.), and even then, we found that commonly prescribe drugs will have that effect in genetically susceptible patients. It has to do with some weird channelopathy of the slow potassium channels in the myocardium and these folks will just drop death from a malignant dysrrhythmia. This effect is significantly increased with certain types of medications and macrolides are one of them. Thankfully, the susceptibility due to genetic predisposition is very rare, so rare, that we don't routinely screen patients for channelopathies, do we? However, a sick heart is a sick heart regardless of the cause and these patients will have higher mortality even if you give them gummy bears for their presbyopia and then an article will be published urging a black box warning for gummy bears. The bottom line is that the possible harm (extremely unlikely) most be weigh with benefits (more likely) and to ask the questions: Is the patient at risk? Taking other QT prolonging meds? Is there history of sudden cardiac death in the family? - In the very few cases with a positive answer, a screening EKG should suffice to make your antibiotic choice.

Finally, this black box warning forces the question... Is the FDA black boxing azithromycin b/c a new "safer" macrolide will be soon introduced to the market in-sync with the Azithromycin patent expiration? Hmmmm. I know I am being cynical... :p

Trendelenburg as adjuvant maneuver for hypotensive patients.

A couple of nights ago I saw an 83 y/o lady with septic shock. She presented in the same way the typical septic patient presents - looking bad and with the blood pressure in the toilet. I think her SBP was in the upper 50's. Not good! Her nurse, who is very smart and proactive, quickly started the IV's, hooked the monitor and tilted the bed in Trendelenburg position.

Trendelenburg position, a time-tested maneuver for the hypotensive patients, has been taught for generations of med students and nurses. It is written in text books and very commonly practiced. After all, it makes sense. If the BP is so low and we want to maintain cerebral perfusion and good cardiac output, tilting the head to a lower level than the rest of the body should be good, right? The problem is... that this well-intentioned maneuver does exactly the opposite of what it is intended for.

Let's think patophysiology just for few seconds, shall we?

When a patient is in supine position, raising the legs (and leaving the trunk flat) will cause an "auto-transfusion" with blood from the legs entering the central circulations and according to the Frank-Starling law, the heart will be able to pump that extra volume resulting in a temporary increase in cardiac output. (http://www.annalsofintensivecare.com/content/1/1/1  middle of the page) The key word here is "temporary", baroreceptors make this a short-lived effect and the only use of this maneuver is to see if the patient will respond to volume loading. So, what happens when the legs go up and the head goes down? There are multiple things that occur... There is an increase of blood flow to the upper body (which is now in the lower level) but this effect is "temporary" because in a few seconds the central venous pressure will increase to a point that arterial flow will inevitably decreased. It basically creates a traffic jam of blood trying to flow back to the heart, but can't b/c the venous pressure is high. This is the same thing that happens when you do the yoga head stand and feel like your eyes will pop out of your face, that is the increase venous pressure, the same phenomenon happens in Trendelenburg just not as severe. Also, the effect of gravity will push the abdominal contents against the diaphragm reducing thoracic expansion, causing increased intrathoracic pressure decreasing venous return even more, preload and finally, cardiac output. Therefore... Trendelenburg is not an effective way to improve heart and cerebral perfusion, it actually lowers cerebral perfusion and cardiac output potentially making things worse.

Now,  back to our lady...

When I came to the room, I placed her supine and even raised the head slightly (10 degrees is more comfortable than flat), grabbed the ultrasound to look at her IVC and noted it was almost collapsing. 5 liters of crystaloids later, IVC was full, SBP was in the low 100's and she looked a lot better.

Take home points

- Trendelenburg does not improve hemodynamics in hypotensive patients and it may cause harm.
- Other ways to assess fluid responsiveness should be used to guide resuscitation.
- Ultrasound ROCKS!
- It is time to tackle this "Tren" myth and share the love with other colleagues for the sake of our patients.


Here are just few reviews I found, in case you need some more reading about this topic.

http://www.annalsofintensivecare.com/content/1/1/1
http://www.ncbi.nlm.nih.gov/pubmed/467083
http://ajcc.aacnjournals.org/content/14/5/364.full
http://www.cjem-online.ca/v6/n1/p48

When you feel you are losing it, watch this...

In the hectic and crazy environment of the emergency department (read practice of medicine too), it is very easy to lose your connection with the human part of medicine. On daily basis we see pain, suffering, frustration, anger, hopelessness, and all kind of emotions reflected in the face and voices of our patients. We see diseases, they see a truncated future. We talk about treatment, they talk about how this is going to change their life.

Let's not forget why we went into this field, why we go back to that our second home called "hospital" day after day, night after night....  It's for them.

Watch these videos, then forward them to all health care professionals you know.

Have a good shift.

https://www.youtube.com/watch?v=cDDWvj_q-o8

http://www.youtube.com/watch?v=fn_71-bMwmw

Vasopressin, Epinephrine & Steroids for Cardiac Arrest!

Vasopressin, Epi and Steroids for Cardiac Arrest !

Wow... for this first post. I have something very VERY important.

Just few days ago in JAMA, an article from researchers in Greece (out of all places) that may spin the wheel in the ACLS world. Combination of Epi, Vasopressin & Steroids for cardiac arrest. Patient who had the combo were more likely to leave the hospital with better neurological outcome. GREAT !

I am going for this in my next cardiac arrest case and then report back what happens.

Thanks to the Greek Gods of research !

http://jama.jamanetwork.com/article.aspx?articleid=1713589

Blog Number 1 - Why a blog? Who am I?

Hello everyone and welcome to my blog.

About me: In 2002, I started my career in medicine as Family Physician, but saw the light soon after residency and followed that with a 2-year EM fellowship completed in 2006. I currently work in the trenches, jumping from country to country, blending in with the local talents in Emergency Medicine and Critical Care and learning their techniques and skills. Over the years, I have worked in very diverse settings, from large university centers to rural and remote locations covering different countries in 4 continents.

Why a blog: For the last 10 years I have been collecting articles, pictures, EKG's, commentaries, editorials and links containing useful information and teachings about Emergency Medicine and other related topics. I have also shared many of them by email to a small group of fellow physicians, nurses, medical students and other health care professionals interested in these topics. In the current era of easy access to information, the only logical move forward is to start a blog. So, this is it! Feel free to comment and add other information that will enrich the experience of every one visiting. You can also contact me using my profile page or at adan.atriham@gmail.com. I strongly believe that by sharing knowledge and opinions is the only way to improve the delivery of medical care to our patients across the globe.

Disclaimer: I have no relationships with any institution, company or association, and receive no funding or financial contribution from anyone. Whatever I write in this blog is purely based on my reading of the evidence (when available) and/or personal opinion based on my experience. Any cases discussed in this blog are cases in which I have been involved as primary provider or in consultation with other colleagues in any of the multiple hospitals I have practiced or currently practice, and all identifiable information was been removed or modified. Although anyone is welcome to visit, this blog is mostly written for health care professionals and it is not my intention to provide treatment advice but rather a source of useful information that when used with clinical judgment may help improving patient care.