The Science of Getting an IV & Collecting Blood

The case was a young trauma victim, he wasn't that sick, but sick enough to get admitted for observation. As part of the trauma protocol we collect blood for labs, type and screen and the usual stuff. Primary survey completed, we had a nice 16 g cannula in his left AC fossa but blood had not been collected yet. The lab tech arrived and was preparing to stick the patient in the R arm when I asked him. Why don't you take the blood from the cannula? - I'm not allowed to do that. He replied. I like to avoid unnecessary pain to my patients whenever possible so I reapplied a tourniquet to the L arm, pulled 3 cc of blood to discard, then collected the blood directly into the tubes. As I was doing that, the ED chief nurse saw me from across the room and almost had a stroke. She went into a rant about how this was a violation of the protocols and yara yara yara... To my amusement, she took the tubes I had just collected from that freshly-started IV and trash them into the sharps container. Then she order the lab tech to stick the patient again in the other arm for a "correct" blood sample. This was a senior nurse and I just couldn't believe she would do that. What is the difference from that blood to the blood in the other arm?!

So I did a lit search about this topic and found some interesting data. 

- The cannulas are made with soft plastic that remains open by the positive pressure exerted by the infusing fluid, the walls tend to collapse if too much negative pressure is exerted, this causes turbulence and higher rate of hemolysis. This hemolysis is more likely to occur using the larger vacutainer tubes of 10 cc because of higher negative pressure early in the draw or when using a syringe and pulling too hard on the plunger. So if you use a syringe, pull the plunger just a little bit until you see blood flowing into the barrel and then continue gently, and for the vacutainer system, use the 5 ml tubes to minimize hemolysis. 

- And what is the deal of tapping the site to "pop" the vein into view? That doesn't work, the skin gets red but the vein doesn't change in size and it also can cause hemolysis inside the vein, so let's not do that either. 

- Already inserted cannulas can be used to collect a blood sample even when IV fluids of medications have been infused through it. The only caveat is that for glucose containing fluids it is recommended to wait 3 minutes after stopping the infusion. When using the inserted IV, "washing" the cannula with 5 times its capacity and discarding that blood will eliminate any possibility of contamination. The volume capacity of a 22g cannula is about 0.05 ml and for a 14g  0.15 ml (yes, go ahead and measure it), therefore drawing 1 ml is technically enough, but get 2 ml and no one will argue.

- If you have a prolonged vein hunt for more than 2 minutes, go ahead and get the cannula in, remove the tourniquet, elevated the arm and then bring it down again to allow "fresh" blood into the extremity, reapply the tourniquet and then collect the samples. This is particularly important if you use venous lactate  in sepsis screening to avoid false positive results. 

- Follow this order when filling up the tubes: Blood cultures -> Lactate -> Coagulation -> Serum -> Heparin -> EDTA. This will minimize the chance of contamination, false positives, hemolysis and sample clotting. 

- Don't overfill, shake too hard or drop the tubes; and if you open the tubes transfer the blood from the syringe, do it without the needle.

And this is the summary of all of these articles. If you have a couple of hours and there is nothing on TV, go ahead and read...

http://bmhlibrary.info/11174369.pdf
http://www.ncbi.nlm.nih.gov/pubmed/15565033
https://www.futurelabmedicine.org/pdfs/LMBP_ReducingHemolysisSummary.pdf
http://www.who.int/injection_safety/phleb_final_screen_ready.pdf

And before I go, a final advice for my fellow physicians. If you think that starting IV's and collecting blood is the nurses' job, then you are missing the critical concept of team work. As leader of the team you should know how to do this and every other procedure in the ED; from starting lines, mixing drips, work up the pumps, etc. This will not only benefit the patient, it will also earn some golden points with the rest of the team. So pull up your sleeves and get busy.  

Wellen's Syndrome... an EKG Finding Not to Miss!

Let's say you're working away in the emergency department and you see a 35 year old man complaining of chest pain for about 2 hr. He does not have a significant PMHx, he is mildly obese and smokes a pack a day, the history is not totally convincing for ACS and when he arrives to the ED the pain has resolved. Sounds familiar...? - We probably see a 10 of those per shift! The protocol says, everyone who says the words "chest" and "pain" in the same sentence gets an ECG at triage. The nurse brings it to you and this is what you see.. (sorry for the shadows, but I couldn't find the right angle)

Hmmmm... A 10 second view shows sinus rhythm, a little slow, the voltages are a bit low in the limb leads. There are some ST-T changes that don't look quite right with T wave inversions in the anterior and lateral leads, with similar milder changes in the inferior leads. The J point seems to be isoelectric and there is some "eyeballed" QT prolongation (R to R seems longer than the twice the length of the QT). The protocol also says that in the absence of contraindications everyone gets hooked to the monitor, oxygen by nasal cannula, aspirin, labs, CXR, maybe NTG. (Yes, I know, and before you start going at it, I am trying to change that oxygen mandate in my department; but it is hard to change protocols!) You do a physical exam which, as in most cases, does not reveal anything significant. Few minutes later the labs come back with negative cardiac markers, his CXR looks fine and he remains pain free. The repeat EKG looks like this... The changes practically resolved!

Now what?! What's the deal here? This dude has dynamic EKG changes, but he is pain free, markers are normal, and now everything seems to be OK. Right? - WRONG! This guy is in deep doo-doo if you don't do the right thing. And the reason you should be scared is b/c he has Wellen's syndrome. 

Wellen's syndrome is an electrocardiographic phenomenon seen in critical obstruction of the LAD. Described in the 1980's, Wellen's has 2 types, type 1 has biphasic T wave in leads V1-V4, with the type 2 having deep T waves inversions. Other characteristics are no precordial Q wave and no loss of R wave progression. (Here is a type 2, note the deep TWI in anterior leads)

So, what happened to our patient? - I called cardiology and said something like this: "Sir, I have a 35 y/o with Wellen's, currently chest pain free, with negative cardiac markers. Do you want to see him here in the ED or in the CCU?" The cardiologist seemed to be in a good mood that day and didn't give me any grief. Patient went up to CCU and booked for cath the next day.

Now, putting it all together. What you need to know about Wellen's

- Recognize the pattern of biphasic T wave or deep inverted T waves in V1-V4

- It means high degree of obstruction in the LAD

- DO NOT send this patients for stress test. It will precipitate an AMI

- These patients need admission and early revascularization

- Do not miss it. This is a "pre-infarct" phenomenon. If the patient goes home, he/she will progress into an anterior MI, and that is considered not good.

For more reading...

- de Zwann C, Bar FW, Wellens. Characteristic electrocardiographic pattern indicating a critical stenosis high in the left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982; 103:730-736

- Tandy TK, Bottomy DP, Lewis JG. Wellen's syndrome. Ann Emerg Med 1999; 33:347-351 (http://www.ncbi.nlm.nih.gov/pubmed/10036351)

- Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med. 2002; 20:638-643. (http://www.ncbi.nlm.nih.gov/pubmed/12442245)
- http://www.consultantlive.com/cardiovascular-diseases/content/article/10162/2158916
- http://www.consultantlive.com/cardiovascular-diseases/devil-t-wave-wellens-syndrome

In honor of Dr Wellens

http://www.ficemaastricht.org/index.php?page=speakers&sid=HW

Optimal Treatment for Post-Cardiac Arrest Patient

OK... it's been 2 weeks and it is time for another post.


Few days ago I had an interesting conversation with one of the cardiologist at one of the hospitals I'm working. The case was a 46-year-old post cardiac arrest patient. He had a witnessed collapse at home.  Paramedics arrived shortly after and began ACLS protocols. He was shocked seven times because of persistent VF and received five rounds of epinephrine with ROSC during transfer. Upon arrival his vitals were not terribly bad he was slightly hypotensive and tachycardic, but he's electrocardiogram didn't have ST elevation, but mild ST depressions in the inferior and lateral leads, so he didn't meet criteria to activate the cath lab as a code STEMI. However, this was a post arrest case and based on what I have seen in current literature, he has the best chances of surviving neurologically intact by combining hypothermia and catheterization. So I called the cardiologist on call and presented the case, and suggested that he should start making his way in while we start hypothermia and prepare him for cath. This conversation didn't go well at all. The cardiologist almost had a stroke while talking to me on the phone. He argued that there was no indication to go to the Cath Lab in a post cardiac arrest case without ST elevation in the ECG, and if someone agreed to cath this patient, it was the wrong thing to do and yara yara yard. - OK... no problem, thanks so much doc. Next; I called 2 different cardiologists with the same request. "Would you please take this young, post arrest, ST depression patient to cath? - The third cardiologist finally agreed, so we started cooling the patient and rushed to the cath lab before the cardiologist could change his decision... He found a 90% occluded LMCA. 

Unfortunately this is not an uncommon scenario. The cardiologists tend not to cath post-cardiac arrest patients without STEMIs because this group tends to do worse and it looks bad for their numbers. However... there is support for the cool and cath approach for NSTEMI post cardiac arrest patient in their own literature. Check this out, this is from the Journal of the American College of Cardiology, probably the most influential cardiology journal in the world, right up there with European Society of Cardiology and American Heart Association.

http://interventions.onlinejacc.org/article.aspx?articleid=1207384

These are the key points of this article

- The lack of ST elevation in the post arrest 12-lead ECG is not a reliable predictor for the absence of acute coronary disease. 

- The NNT with coronary angiography in a post-cardiac arrest patient after cardiac arrest to find an acute culprit lesion needing emergent revascularization among those without ST-segment elevation is, in fact, just 4 patients.

- "Resuscitated cardiac arrest victims without an obvious non- cardiac etiology should undergo emergency coronary angiography and, where indicated, percutaneous coronary intervention. If comatose, they should receive concurrent therapeutic hypothermia. Such an approach can double long-term survival rates among those successfully resuscitated after out-of-hospital cardiac arrest".

Therapeutic hypothermia and early catheterization with PCA when needed, is the best chance for a good outcome in post-cardiac arrest patients regardless of the initial ECG. If they argue otherwise, just refer them to their own journal. However, It will be wise to sit with the cardiologists at 3 pm, have a coffee and agree in a plan for these type of situations and have it all sorted out, so when the ambulance arrives at 3 am things are easier for everybody.

A nice review article with everything included: http://www.epmonthly.com/www.epmonthly.com/features/current-features/post-cardiac-arrest-care/?utm_source=EPI+Global+Briefing+0412+3-19-14&utm_campaign=Global+Briefing+3_27_14&utm_medium=email

I am allergic to Penicllin... - Oh, are you really?

You: Sir, are you allergic to anything?
Patient: Oh yeah, I am allergic to Penicillin.
You: What happens when you get Penicillin?
Patient: I don't know, my mom told me I am allergic to it.
You: Did she tell you why or what happened to you?
Patient: Uhhh. Not really, but I think I stopped breathing.
You: Really...?  o_0

Well, you get the idea...

How many patients do we see who say they are allergic to PNC but there is no convincing proof they really are? About 8% of the US population claim being PNC allergic; but skin testing to identify true IgE-mediated allergy is rarely done. Anaphylaxis, the one reaction we care about, is actually quite rare in these patients. In May of this year, in the Journal of Allergy and Immunology, a study was published about this issue (http://www.jaci-inpractice.org/article/S2213-2198%2813%2900123-2/abstract). From 2010 to 2012, 500 patients with histories of penicillin allergy (based on diagnoses recorded in their records) were skin tested in a California allergy department. Negative tests were followed by 1-hour observed oral challenges with amoxicillin. Only 4 patients reacted to one of the two skin-test agents, and another four exhibited positive objective symptoms after oral challenges but none of these reactions were life threatening or required epinephrine, NONE! Fewer than 1 in 50 patients with penicillin allergy histories were truly allergic. Note that this is an allergy clinic, which already selects a higher allergic risk population compared to the undifferentiated patient we see in the ED.

We should stop accepting penicillin allergy history as a reason for lifelong avoidance. All drug reactions should be documented carefully. Patients with severe delayed reactions such as Stevens Johnson syndrome, drug reaction with eosinophilia and systemic symptoms (DRESS), or hemolytic anemia should never be challenged or tested; those with mild delayed reactions probably can undergo oral challenges. For those with potential IgE-mediated reactions (i.e., hives, edema, or other symptoms of anaphylaxis occurring within 1–2 hours), penicillin testing followed by oral challenge is safe and effective. However, are we going to do this in the ED? Abso-freaking-lutely NO. But we can suggest they follow up with their PCP for testing.

I guess for us in the ED, the main issue I hear a lot of noise around, is the cross reactivity with Cephalosporins. In fact, many EHR's flag red lights and sirens when ordering Cephalosporins in patients reporting PNC allergy. Even with the assumption that the patient is truly allergic to PNC, is there a real risk? - The answer is yes, but it is sooooo very small that the meningitis is more likely to kill the patient than the shot of Ceftriaxone. Here is the evidence (http://www.ncbi.nlm.nih.gov/pubmed/7697478) "It is safe to administer cephalosporin antibiotics to penicillin-allergic patients and penicillin skin tests do not identify potential reactors", (http://www.ncbi.nlm.nih.gov/pubmed/16451776) "The widely quoted cross-allergy risk of 10% between penicillin and cephalosporins is a myth". And one more... (http://www.ncbi.nlm.nih.gov/pubmed/16564780) Out of 3.3 million (yes, million) who received PNC, 506,000 received a cephalosporin. The risk of anaphylaxis for those who had a prior event with PNC was < 0.001% after receiving a Cephalosporin.

So, these are my 2 conclusions:

1.- Patients who claim being allergic to PNC, unless they have a good history for skin/airway/hematologic reaction, are probably not.
2.- Cephalosporins are generally safe in patient with history of PNC allergy.

Thank you very much, stay tuned for more myth busting reading.

Fever is HOT !

As many of you (who have time to read my notes) know, I have a little fascination with pediatric fever. I like the topic, reading about the body's response to infections is very interesting and the more I read about it the more I believe that treating fever does more harm that good (in most cases anyway). The ability of the body to heal it self can not be undermined. Just think about coagulation homeostasis, what a complex and yet perfectly balanced system that keeps us from bleeding to death and not dying from clotting. In the same way, the generating of fever is part of the immune system's response to infections improving chemotaxis of white cells, killer T-cell action, antibody production and many other protective immune functions... could the body be wrong by increasing body temperature? - I don't think so.

Few days ago I was searching for some articles about pediatric fever and came across this blog (http://lifeinthefastlane.com/2013/07/fever-friend-or-foe/?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+LITFL+%28Life+in+the+Fast+Lane%29) talking about how fever was used to treat neurosyphilis in the 1910's and how a Nobel prize winner cured some patients from paralytic syphilis by infecting them with the high-fever illness, malaria! Gonorrhea was also treated in the hyperthermia chamber with high cure rates. Another clear example that treating fever may cause more harm than good is the post vaccination period in children. It is very common to have parents rushing their kids to the ED because of fever after getting vaccinated. There is a very well done study done in the Czech Republic that evaluated the effect of antipyretics on the immunogenicity of vaccines (http://www.sciencedirect.com/science/article/pii/S0140673609612083) The conclusion was that antipyretic use was associated with lower antibody levels for many vaccines, decreasing the protective effect of the immunizations. Hmmm, maybe we should start telling parents not to treat fever!

These examples invariably lead to the question... How (and when) did fever become a cause of panic and the evil symptom modern medicine aims to treat?  As more and more bacterias develop effective ways of resistance to multiple antibiotics and less and less new effective antibiotics are developed, I just wonder... will the days when induced hyperthermia become an effective therapy be back anytime soon? I believe they will.. just as induced hypothermia has become standard of care in post-cardiac arrest patients, induced hyperthermia will take the medicine world by storm in a not-too-far distant future. Although too many questions remained unanswered on type of infections that will benefit, degree and length of hyperthermia, whole body vs partial, technique to increase body temperature, protocols, etc. Therapeutic hyperthermia will bring some heat to the traditional thinking of total fever control for infectious diseases. I just need to develop a machine that safely increase temperature to a level enough to kill the bugs and yet prevent the brain from cooking. Anyone wants to take this with me?

Kayexalate, would you like it orally or rectally? - NO THANK YOU !

Few days ago during a night shift, I saw an elderly gentleman from the nursing home who had a potassium of 6.9 mEq/L, among other lab abnormalities. His EKG had some tall T waves, but otherwise, he was asymptomatic. We proceeded to do the usual stuff; calcium, insulin, glucose, albuterol, IVF and some furosemide. We called for a monitored bed and when the patient went up, shortly after I got a call from the floor nurse asking why we didn't give Kayexalate to the hyperkalemic patient. I saw this as an opportunity to educate about how uneffective Kayexalate is and the possible risks of using this ancient and mostly unproven therapy, so I gladly explained that to the nurse. Few minutes later I got a phone call from the hospitalist asking the same question, "why didn't you give Kayexalate to the hyperkalemic patient?" - Now I am thinking... The nurse not only didn't believe me, she called the hospitalist at 3 am to tell him about my terrible omission of therapy! Once again, I tried to explain my reasons for not giving the resin. Dr X, an internist, proceeded to give me a physiology lecture about potassium metabolism and elimination. I politely listened, thanked him for his time and at the end told him that he may want to read what the nephrology literature says about this topic.

I really thought this Kayexalate issue had been put to rest few years ago. Why are we so hard to break old habits? This wouldn't be the first time; after all, medical science has had many bloopers when it comes to therapies, things we thought were good for our patients that were later proven to cause harm. Remember Thalidomide, HRT, Xigris..? It is wise to keep an open mind and look for the evidence behind our practice. So, let's see what the literature says about Kayexalate.

Sodium polystyrene sulfonate, AKA Kayexalate, made its debut in 1957 for the treatment of hyperkalemia. This resin was initially used alone but it caused severe constipation and colonic necrosis, then sorbitol was added as a cathartic. Although less frequent, the combination still has reports of colonic necrosis, perforation and poor outcomes related to its use. That's the reason why in 2009 the FDA issued a black box warning for Kayexalate. I bet you didn't see that one coming, did you? But does it work to reduce potassium? The short answer is NOT really. However, I will go over the long answer. There are only 3 paper in the literature that support the use of Kayexalate: 1) Flinn RB et al. Treatment of the oliguric patient with a new sodium-exchange resin and sorbitol; a preliminary report. N Engl J Med. 1961 Jan 19;264:111-5. This included 10 patients who received potassium free diet + resin/sorbitol. The potassium decreased 0.5 mEq in 24 hrs, and no control group.  2) Scherr L et al. Management of hyperkalemia with a cation-exchange resin. N Engl J Med. 1961 Jan 19;264:115-9. This one had 32 patients with renal failure, all received potassium free diet and Kayexalate oral or rectally. The average reduction in serum potassium was 1 mEq in 24 hr. Again, no control group.  3) Gruy-Kapral C et al. Effect of single dose resin-cathartic therapy on serum potassium concentration in patients with end-stage renal disease. J Am Soc Nephrol. 1998 Oct;9(10):1924-30. This one took 6 patient with renal failure and found no change in serum potassium levels at 12 hrs, and not surprising, this one had no control group either. Although this last study could be seen as a negative study, it is frequently cited as a reason to use the resin. But that's it…! The evidence to support the use of Kayexalate is based in 3 poorly done studies, with the grand total of 48 patients and no control group in any of them. Really… that's it!

And now for the grand finale…. In 2010 the nephrologists digged deep into this literature, which wasn't that hard b/c there is no much of it, and came to the same conclusion published in this paper: Sterns RH et al. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective? J Am Soc Nephrol. 2010 May;21(5):733-5. (http://www.ncbi.nlm.nih.gov/pubmed/20167700 and http://jasn.asnjournals.org/content/early/2010/02/18/ASN.2010010079.abstract) If kayexalate and sorbitol were presented to the FDA today, they would likely not be approved. “It would be wise to exhaust other alternatives for managing hyperkalemia before turning to these largely unproven and potentially harmful therapies".

There you have it… From the Nephrologist's mouth; another myth debunked. Please please pleeeeeease…. forward this post to all your colleagues, and once you are at it, send it to your grandparents, soccer team and the neighbors. It is time to stop using this therapy and get on board with the current times.

Really... A Kayexalate coupon?!

Even the cartoons need to change!

In a side note: Thank you to all my friends at VBMC for treating me so well, to the folks in King Faisal University Hospital for putting such a great conference and letting me be part of it and to my buddies in London for making it my second home. You all know who you are...

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