Emergency Radiology and Pregnancy

My apologies for the delay in posting something new, but this topic required a lot more reading than initially expected. There is a lot of information from very diverse sources, not just medical imaging literature but also from genetics, physics and the energy industry as well. Very interesting stuff!

The pregnant patient is, and will always be, a complex patient. The presentation of life threatening diseases is often atypical, symptoms that could be part of a normal pregnancy may also indicate serious pathology, the physiology of pregnancy is different from a non-pregnant female and to make things even more complicated, there is a little human being inside! No wonder why the sick pregnant patient in the ED scares the socks out of us. We all use our clinical acumen but that is often not enough to decide sick-or-no-sick, and we must rely on imaging technology to aid in the diagnosis. There is handful of non-pregnancy related diagnoses that create all the problems and split hairs, these include appendicitis, renal colic, ovarian torsion, hemorrhagic ovarian cysts, pulmonary embolism and trauma. It is well known that whenever possible, ultrasound is the modality of choice when it comes to imaging the pregnant patient; unfortunately, it is not always conclusive and CT scan becomes the better choice. That's when the "radiation talk" should take place. I have heard all kind of crazy things about this, mostly due to lack of information in patients and even providers. Therefore, I would like to cover some basic physics about radiation and its effects, just to put things in perspective.  It will not make you a physicist, but you can sound like one when talking to the radiologist, and that's very useful. Shall we...?

Fact number 1: Radiation comes from everywhere and everything; from natural sources like air, water, food, plants, ground and cosmic; as well as artificial sources like the electronics we use everyday, buildings, occupational exposures, nuclear and medical imaging, etc.

Fact number 2: There are several units to measure radiation. Depending on which system is used in the country you live in, there are Rads/Grays and Rems/Sieverts. 1 Rad = 1/100 Gray and 1 Rem = 1/100 Sievert. For the purpose of this review, it is worth remembering Grays and Sieverts. A Gray (Gy) is a measure of absorbed ionizing radiation which is equal to 1 Joule of energy release in 1 kg of mater. A Sievert (Sv) is the unit of the effective dose of radiation that has a biological effect on tissue, 1 Sv is equal to effect of 1 Gy over the exposed tissues multiplied by the specific weighting factor. If this sounds too complex (and believe me, IT IS) just remember that a Gray is the amount of radiation received by the tissues and a Sievert is the unit for the effects of 1 Gray of radiation in humans. Although technically are not the same, for practical purpose they can be thought as similar units.

Fact number 3: The average dose of background radiation a human accumulates just for being temporary habitant of this planet is somewhere between 2 and 7 mSv (mili-Sieverts) depending on location and altitude. There are high radiation locations in areas of nuclear disasters, natural occurring "leaks" from the earth, mines and high altitude.

Fact number 4: From the different types or radiation, ionizing radiation is the one used in medicine. Its ability to pass through tissues of different densities makes it ideal for imaging technology and treatment of cancers. The problem is that as it goes through to the tissues, it deposits enough energy to brake molecular bonds and displace electrons from atoms creating free ions (therefore the name ionizing); this results in damaged bonds in the DNA of living cells.

Fact number 5: In industrialized countries, the most common sources of artificial source of ionizing radiation is medical imaging with an average of 3 mSv per year per person (world's average is 0.6 mSv) and air travel with 2.1 mSv per year. Of note, heavy smoking (1 pack per day) results in radiation dose of ~160 mSv per year directly into the lungs! (If you smoke, you need to stop)

Well... I think that's enough physics for one day! Now let's apply these facts to the medical imaging in humans, including unborn babies.

We just learned about the effects of ionizing radiation in living cells and that we all are exposed to radiation from multiple sources at any given time. Then why aren't we all dropping death with cancers of all types? - Well, that is because there is an extremely sophisticated and highly specialized enzymatic complex system that detects, repairs or destroys damaged cells. This awesome system corrects billions of DNA mishaps a day and maintains cellular functions. Ionizing radiation in high doses, and specially after repetitive exposure, can eventually overwhelm this mechanism and lead to various types of malignancies. The fast mitotic fetal cells are particularly vulnerable to these effects from radiation, therefore is a good idea to limit fetal exposure whenever possible.

I found this table with the average dose of radiation from different studies, their equivalent to background radiation in years and its risk for malignancy

Too much is said about the fetal radiation risks for various types of imaging technologies derived from phantom models, animal and human observational studies; all thrown in the same bowl with extrapolated nuclear bomb survivors and nuclear disasters data. The result is an estimation of risk, but let's be clear about something... No one has solid, indisputable human information with a dosimeter next to a developing fetus to accurately measure radiation doses in-utero and its effects based on randomized studies (and we never will). All of the current available recommendations are predicated on estimated risks based on less-than-perfect data. Having said that, this is all we have and it seems to be enough to draw some conclusions.

The background dose of radiation for 9 months of pregnancy is estimated at 0.5 to 1 mGy, and the threshold for increased risk of fetal anomalies or pregnancy loss is 50 mGy (5 Rads) or 50 mSv (5 Rems). Standard radiological tests produce radiation doses far below the 50 mSv threshold. The aggregate risk for spontaneous miscarriage, major malformation, mental retardation and childhood malignancy in the general population is estimated to be about 28.6%. A dose of 50 mSv of ionizing radiation will increase this risk to approximately 28.8%. Specifically about childhood cancer, defined as any cancer with onset before age 15, the most common being leukemia, the average risk of leukemia in general pediatric population is about 0.036% (3.6 per 10,000), exposure to 50 mSv will increase this risk to approximately 0.06% (6 in 10,000).  From these statistical models we can conclude that although the risk of negative effects of the cut off of 50 mSv is not zero, it is indeed, very very small. The National Council on Radiation Protection and Measurements, and the American College of Obstetricians and Gynecologists have both agreed that the potential health risks to a fetus are not significantly increased from most standard medical tests. The American College of Radiology (ACR) has also come on record saying that "No single diagnostic procedure results in a radiation dose that threatens the well-being of the developing embryo and fetus" (Hall EJ. Scientific view of low level radiation risks. Radiographics. 1991;11:509)

This table shows the fetal dose of common radiologic tests. All these give less than 50 mSv, so it is safe to say that when we need to image a pregnant patient using ionizing radiation, we can proceed knowing that any of the studies we use in the ED represent low risk.

This next table summarizes the average dose of multiple radiologic studies and the number of studies needed to reach the aggregate dose of 5 Rads (50 mGy/mSv)

And this last table is from the ACR 2013 revision of its practice guideline on imaging the pregnant or potentially pregnant women using ionizing radiation, reaffirms what has been said by other organizations regarding the cut off of 50 mGv as safe level. 

What about contrast? - Well, I did find some useful information about that from the ACR 2013 manual on contras media. Basically it says that the water soluble iodinated low-osmolarity contrast media (the one use currently) does cross the placenta but there is no current evidence of mutagenic or teratogenic effects from it. As far as the effect on neonatal thyroid function, the document says that the amount of contrast in the fetal circulation is small and transient, and there are no reported cases of neonatal hypothyroidism in babies whose mothers received this type of contrast and the FDA has given it category B status. The ACR's recommendation about the Gadolinium-based contrast media (GBCM) used in nuclear medicine studies is not as strong. It says that although there have been no know adverse effects to human fetuses by the use of this agent, there is only one study of 26 pregnant patients who were exposed to Gadolinium during the first trimester, none had teratogenic nor mutagenic effects of the progeny. Therefore, the use of GBCM should only be used when the benefits justify the potential risk to the fetus. 

OK... are you with me so far? - Good! Let's now get practical and put all this theory where the rubber meets the road, at the bedside of the pregnant patient with a potentially serious diagnosis.

Let's start with the rule-out appendicitis case and the ultrasound comes back with something like this "Appendix not seen, acute appendicitis cannot be excluded, consider pelvic pathology... clinical correlation required". Now what? - Sure, you can try to put your pregnant patient in the MRI for 30 minutes and hope for a clear diagnosis; however, MRI is not as sensitive nor specific compared with CT, thus resulting in equivocal results, and most radiologist are far better diagnosing acute appendicitis on CT than MRI. CT with oral and IV contrast is the better choice, and the 25 mSv dose of radiation are still considered relatively safe by ACR and ACOG. Now the conversation with the patient should include the following... If this is acute appendicitis and we don't find out on time and it ruptures, there is between 6-37% chance for fetal loss, maternal morbidity and mortality range around the 5% and 1% respectively. and the risk of the radiation dose of the CT abd/pelvis for anomalies, fetal loss or childhood cancer is less than 1%. It seems clear that scanning is the best option. 

Urolithiasis with renal colic is the most common non-obstetric diagnosis requiring hospitalization, affects about 1 in 1500 pregnant patients and it is often confused with appendicitis, diverticulitis, ovarian pathology and placental abruption. Ultrasound is first line test to diagnose urolithiasis during pregnancy. When the stone is visualized that's great, but when all you see is hydronephrosis it is hard to tell if that is the hydronephrosis of pregnancy or due to a distal obstruction. The good news is that about 60-80% of stones will pass with conservative management, the bad news is that 20-40% will not and urologist use size of stone and location to determine treatment options. MRI is good to see hydronephrosis but not so much stones, so it doesn't really have significant advantage over ultrasound. Intravenous pyelogram has fallen out of favor because of the 50% higher radiation dose compared with CT scan and it only provides imaging of the urinary tract. CT scan again comes as top option for complicated cases of urolithiasis because of its high sensitivity and specificity, and ability to screen for other intra abdominal/pelvic pathology. 

The pelvic pathology including ovarian torsion, adnexal mass, hemorrhagic cyst and degenerating fibroid are best seen with ultrasound, so no surprises here. However, in late pregnancy the gravid uterus may obscure adequate view with the ultrasound. The MRI without contrast could be used in the stable patient. CT with IV contrast becomes the imaging modality of choice in the unstable patient with hemoperitoneum.

Pulmonary embolism is, on it self, a monster topic which becomes even more monstrous in the pregnant patient. With a mortality approaching 15% and significant morbidity of anticoagulation, we must get this right in a timely fashion. There are several protocols including trimester adjusted D-dimer + leg ultrasound in leu of pulmonary imaging. In patient with symptoms suggesting PE and (+) US for DVT, most will go ahead and treat; but when this approach is not diagnostic, pulmonary imaging becomes mandatory and the options are CT pulmonary angiography (CTPA) vs V/Q scan. The ACR rates both studies as adequate in the pregnant patient with radiation doses below the 50 mSv limit. The American Thoracic Society in its 2011 practice guidelines recommends plain chest x-ray as the initial radiation-associated step. If the CXR is normal, proceed with the perfusion phase of V/Q scan followed by the ventilation portion if abnormal. If CXR is abnormal, then CTPA is recommended. The algorithm looks like this...

The problem with this approach is that if the V/Q is inadequate or non-diagnostic (and many of them are), then you still have to proceed with CTPA. The advantages of CTPA is that it can also provide alternative diagnosis (i.e. pneumonia) and is more widely available compared with a V/Q scan. The fetal radiation doses of both studies is fairly comparable with an average of 0.2 mSv for CTPA, 0.12 for the perfusion-only V/Q and 0.2 for the ventilation portion of the V/Q scan. The remaining issue to discuss about CTPA is the radiation exposure to the hyperplastic breast tissue of the pregnant patient, which is said to increase life time risk for breast cancer in about 1%. Breast shields and timed beam techniques can significantly lessen this exposure.

The final diagnostic dilemma to review is trauma. This is the easy one because everyone agrees that when it comes to radiology studies, you just do it. Trauma is the number 1 reason for non-obstetric mortality during pregnancy, and unless you are ready to do a perimortal c-section, treating mom is the best way to treat baby. The pregnant trauma victim should be imaged just as the non-pregnant with x-rays, CT or angiography when required. Sure, you take a quick look with the US to check on the fetus and the placenta, but don't get hang on that screen while the mom is bleeding out, and remember that every pregnant trauma victim beyond 24 wks gestation once stable, should be placed in continuos cardio-tocographic, which is the most sensitive way to diagnose placental abruption. It is possible that mom may require multiple studies that may add up radiation doses of > 50 mSv and rarely > 150 mSv, and someone needs to keep track of what studies have been done and what studies are still needed. In such cases with high fetal exposure doses, therapeutic abortion should be discussed with the patient.

Wow... you are still reading! I am sorry this topic is too long, but I think it contains useful information that can be applied anytime when you pick up a chart saying "20 wk pregnant with abdominal pain". Now, it is time for final points.

Pregnancy test. The ACR says that for negligible risk examinations like CXR or extremity plain films, pregnancy test is unnecessary. Documentation; when higher risk examination is needed make sure to document clearly and completely. Tell the chart you have discussed alternative diagnostic options with the patient, mention the risks of doing and not doing the test, and what you feel is in the best interest of mother and baby. Finally, remember that avoiding radiologic tests in a potentially life threatening condition in order to avoid fetal exposure to ionizing radiation is not going to score you any points when you end up with a dead mother, so do what it right for your patients.

References:
http://pubs.rsna.org/doi/full/10.1148/radiol.2481071451
http://pubs.rsna.org/doi/full/10.1148/radiol.2312030767
http://www.acr.org/~/media/9e2ed55531fc4b4fa53ef3b6d3b25df8.pdf
http://www.sievert-system.org/WebMasters/en/mesure.html
http://hyperphysics.phy-astr.gsu.edu/hbase/nuclear/radrisk.html#c1
http://www.radiologyinfo.org/en/safety/index.cfm?pg=sfty_xray#part6
http://www.radiologyinfo.org/en/safety/index.cfm?pg=sfty_contrast#part7
http://hps.org/documents/pregnancy_fact_sheet.pdf
http://hps.org/physicians/documents/Radiation_and_Pregnancy.pdf
http://www.acr.org/~/media/ACR/Documents/PDF/QualitySafety/Resources/Contrast%20Manual/2013_Contrast_Media.pdf/#2013_Contrast_Media_Manual.indd:.27754:10189
http://www.nrc.gov/about-nrc/radiation/health-effects/radiation-basics.html
http://emedicine.medscape.com/article/455830-overview
http://www.medscape.com/viewarticle/812189_2?nlid=38923_541
http://www.acog.org/Resources_And_Publications/Committee_Opinions/Committee_on_Obstetric_Practice/Guidelines_for_Diagnostic_Imaging_During_Pregnancy
http://en.wikipedia.org/wiki/Background_radiationhttp://www.aafp.org/afp/1999/0401/p1813.html
http://www.thoracic.org/statements/resources/pvd/evaluation-of-suspected-pulmonary-embolism-in-pregnancy.pdf
http://www.ncbi.nlm.nih.gov/pubmed/17620458
http://www.aafp.org/afp/1999/0401/p1813.html

Low Risk Chest Pain and the Accelerated Protocols

This is a monster topic and the pain of our existence in the ED. We see CP patients left and right and some can represent a challenge to even the seasoned clinician. The crushing retro-sternal CP in a 66 y/o sweaty-obese-hypertensive-diabetic-smoker is the easy one, even the intern knows that patient is not going home b/c the probability of ACS is so high, that even normal tests are likely to be falsely negative. The 21 y/o with chest pain and large bruise after being hit with a baseball is going home b/c he doesn't have ACS. Those too are easy... the hard cases are the ones in between, when the story is not totally convincing, the exams is not helpful, the EKG is not conclusive and the patient may have some risk factors or positive family history. As the gate keepers and stewards of the health care system, we must move these patients through the department efficiently and effectively, without missing a single case. Right?

Multiple risk assessment tools have been developed to help us identify low risk CP patients who are safe for discharge and can be followed up as outpatient. Some of these score systems have been validated and the basic idea is to quickly identify patients who are a very low risk for adverse events in a short period of time (usually 2 hrs) instead of the usual 8-12 hr protocols. A key concept to understand is that we do not rule out ACS in the ED, a patient with 90% stenosis can graduated from the department with 3 sets of negative cardiac markers and non-diagnostic EKG's. So we re-stratify patients to a level of risk that is acceptable (and defendable) that will guide further management.

It is not my intention to write a meta-analysis given the heterogeneity of these individual studies in their methodology, protocols and type of biomarker used. But here is a quick summary of some of the main studies evaluating accelerated re-stratification protocols (Rajeev... I hope this answers your question)

The Lancet. March 2011 (http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2811%2960310-3/fulltext) was a prospective validation study of 3582 patient in Australasia using a TIMI score of 0 (http://www.mdcalc.com/timi-risk-score-for-uanstemi/), non-ischemic EKG, negative biomarkers at 0 and 2 hr time. If all of those criteria were fulfilled, these patients were considered safe for discharge. Out of the initial pool of patients, 352 met criteria for discharge and only 3 had a cardiovascular negative outcome within 30 days defined as AMI, need for revascularization or death. This gives a 99.3% sensitivity, a 99.1% NPV and specificity of only 11%.

JAMA, December 2011 (http://www.ncbi.nlm.nih.gov/pubmed/22203537?access_num=22203537&link_type=MED&dopt=Abstract) Another prospective study, done in Germany with 1818 subjects. This study used only highly sensitive troponin I (no scores and no EKG's) at 0, 3 and 6 hrs. At 3 hr, repeat negative troponins had a sensitivity of 98.2% and PPV of 95.8% for ACS, with the 6 hr marker not adding significant extra benefit, making the point that 3 hr markers are as good as the 6 hr.

Clinical Pathways in Cardiology. March 2013. This is an European journal (http://journals.lww.com/critpathcardio/Abstract/2013/03000/HEART_Score_to_Further_Risk_Stratify_Patients_With.1.aspx) and the authors here put forward a new HEART score (http://www.heartscore.nl/score/) applied to patients with an already low TIMI score (0-1) to further identify very low risk patients who are safe for discharge from the ED. This included 8815 enrolled, from which 485 had both a TIMI of 0 and HEART score of 0. From this subset none had a negative cardiovascular outcome at 30 days for a sensitivity of 100%.

JAMA, Internal Medicine. October 2013. (http://archinte.jamanetwork.com/article.aspx?articleID=1748796) This is a randomized, parallel comparison study with blinded outcomes comparing a 2-hr accelerated diagnostic protocol (ADP) including TIMI of 0, non-ischemic EKG and negative biomarkers at 0 and 2 hr, vs standard care (initial negative biomarkers, prolonged observation usually with admission to hospital and second biomarker at 6-12 hr after onset of symptoms). The ADP had 270 pt of which 52 were discharge following the protocol and the standard care group had 272 pt and 30 discharges. At 30 days none of the discharged patients in both groups reported a negative cardiovascular event, making the conclusion that accelerated protocols are as effective and more efficient than standard prolonged observation protocol.

So, now what do we do with this information? Are these accelerated protocols ready for clinical use in the ED? Well... sort of. The good news is that these studies were done in the ED with general population cohorts and not cardiology centers, they have excellent results which can be applied to general practice. The bad news is that the AHA and ACC have not yet come on record with an official opinion about these protocols. However, as more and more patients show up through our doors with CP's the need for more efficient and cost-effective disposition has become imperative. But don't be the odd ball of your group and start doing this alone, take this information and talk to your medical directors and come up with an agreement on how to use these protocols in your departments.

A heart ATTACK !!!

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...