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    Education

    EMplify by EB Medicine

    Take a deeper dive into our peer-reviewed emergency medicine content with the EMplify podcast. Join hosts Sam Ashoo, MD and T.R. Eckler, MD for educational, conversational reviews of current evidence guaranteed to help you make your best clinical decisions. Each high-yield episode gives you practical, time-tested guidance from practicing emergency medicine clinicians and subject-matter experts. Listen and learn!

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    Latest Episodes:
    Episode 24 - First Trimester Pregnancy Emergencies: Recognition and Management Jan 02, 2019
    Show notes

    Jeff: Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, we’re talking about a topic…

    Nachi: … woah wait, slow down for a minute, before we begin this month’s episode – we should take a quick pause to wish all of our listeners a happy new year! Thanks for your regular listenership and feedback.

    Jeff: And we’re actually hitting the two year mark since we started this podcast. At 25 episodes now, this is sort of our silver anniversary.

    Nachi: We have covered a ton of topics in emergency medicine so far, and we are looking forward to reviewing a lot more evidence based medicine with you all going forward.

    Jeff: With that, let’s get into the first episode of 2019 – the topic this month is first trimester pregnancy emergencies: recognition and management.

    Nachi: This month’s issue was authored by Dr. Ryan Pedigo, you may remember him from the June 2017 episode on dental emergencies, though he is perhaps better known as the director of undergraduate medical education at Harbor-UCLA Medical center. In addition, this issue was peer reviewed by Dr. Jennifer Beck-Esmay, assistant residency director at Mount Sinai St. Luke’s, and Dr. Taku Taira, the associate director of undergraduate medical education and associate clerkship director at LA County and USC department of Emergency Medicine.

    Jeff: For this review, Dr. Pedigo had to review a large body of literature, including thousands of articles, guidelines from the American college of obstetricians and gynecologists or ACOG, evidence based Practice bulletins, ACOG committee opinions, guidelines from the American college of radiology, the infectious diseases society of America, clinical policies from the American college of emergency physicians, and finally a series of reviews in the Cochrane database.

    Nachi: There is a wealth of literature on this topic and Dr. Pedigo comments that the relevant literature is overall “very good.” This may be the first article in many months for which there is an overall very good quality of literature.

    Jeff: It’s great to know that there is good literature on this topic. It’s incredibly important as we are not dealing with a single life here, as we usually do... we are quite literally dealing with potentially two lives as the fetus moves towards viability. With opportunities to improve outcomes for both the fetus and the mother, I’m confident that this episode will be worth your time.

    Nachi: Oh, and speaking of being worth your time…. Don’t forget that if you’re listening to this episode, you can claim your CME credit. Remember, the indicates an answer to one of the CME questions so make sure to keep the issue handy.

    Jeff: Let’s get started with some background. First trimester emergencies are not terribly uncommon in pregnancy. One study reported 85% experience nausea and vomiting. Luckily only 3% of these progressed to hyperemesis gravidarum. In addition, somewhere between 7-27% experience vaginal bleeding or miscarriage. Only 2% of these will be afflicted with an ectopic pregnancy. Overall, the maternal death rate is about 17 per 100,000 with huge racial-ethnic disparities.

    Nachi: And vaginal bleeding in pregnancy occurs in nearly 25% of patients. Weeks 4-8 represent the peak time for this. The heavier the bleeding, the higher the risk of miscarriage.

    Jeff: Miscarriage rates vary widely based on age, with an overall rate of 7-27%. This rises to nearly 40% risk in those over 40. And nearly half of miscarriages are due to fetal chromosomal abnormalities.

    Nachi: For patient who have a threatened miscarriage in the first trimester, there is a 2-fold increased risk of subsequent maternal and fetal adverse outcomes.

    Jeff: So key points here, since I think the wording and information you choose to share with often scared and worried women is important – nearly 25% of women experience bleeding in their first trimester. Not all of these will go on to miscarriages, though the risk does increase with maternal age. And of those that miscarry, nearly 50% were due to fetal chromosomal abnormalities.

    Nachi: So can we prevent a miscarriage, once the patient is bleeding…?

    Jeff: Short answer, no, longer answer, we’ll get to treatment in a few minutes. For now, let’s continue outlining the various first trimester emergencies. Next up, ectopic pregnancy…

    Nachi: An ectopic pregnancy is implantation of a fertilized ovum outside of the endometrial cavity. This occurs in up to 2% of pregnancies. About 98% occur in the fallopian tube. Risk factors for an ectopic pregnancy include salpingitis, history of STDs, history of PID, a prior ectopic, and smoking.

    Jeff: Interestingly, with respect to smoking, there is a dose-relationship between smoking and ectopic pregnancies. Simple advice here: don’t smoke if you are pregnant or trying to get pregnant.

    Nachi: Pretty sound advice. In addition, though an IUD is not a risk factor for an ectopic pregnancy, if you do become pregnant while you have in IUD in place, over half of these may end up being ectopic.

    Jeff: It’s also worth mentioning a more obscure related disease pathology here – the heterotopic pregnancy -- one in which there is an IUP and an ectopic pregnancy simultaneously.

    Nachi: Nausea and vomiting, though not as scary as miscarriages or an ectopic pregnancy, represent a fairly common pathophysiologic response in the first trimester -- with the vast majority of women experiencing nausea and vomiting. And as we mentioned earlier, only 3% of these progress to hyperemesis gravidarum.

    Jeff: And while nausea and vomiting clearly sucks, they seem to actually be protective of pregnancy loss, with a hazard ratio of 0.2.

    Nachi: Although this may be protective of pregnancy loss, nausea and vomiting can really decrease the quality of life in pregnancy -- with one study showing that about 25% of women with severe nausea and vomiting had actually considered pregnancy termination. 75% of those women also stated they would not want to get pregnant again because of these symptoms.

    Jeff: So certainly a big issue.. Two other common first trimester emergency are asymptomatic bacteriuria and UTIs. In pregnant patients, due to anatomical and physiologic changes in the GU tract – such as hydroureteronephrosis that occurs by the 7th week and urinary stasis due to bladder displacement – asymptomatic bacteriuria is a risk factor for developing pyelonephritis.

    Nachi: And pregnant women are, of course, still susceptible to the normal ailments of young adult women like acute appendicitis, which is the most common surgical problem in pregnancy.

    Jeff: Interestingly, based on epidemiologic data, pregnant women are less likely to have appendicitis than age-matched non-pregnant woman. I’d like to think that there is a good pathophysiologic explanation there, but I don’t have a clue as to why that might be.

    Nachi: Additionally, the RLQ is the the most common location of pain from appendicitis in pregnancies of all gestational ages. Peritonitis is actually slightly more common in pregnant patients, with an odds ratio of 1.3.

    Jeff: Alright, so I think we can put that intro behind us and move on to the differential.

    Nachi: When considering the differential for abdominal pain or vaginal bleeding in the first trimester, you have to think broadly. Among gynecologic causes, you should consider miscarriage, septic abortion, ectopic pregnancy, corpus luteum cyst, ovarian torsion, vaginal or cervical lacerations, and PID. For non-gynecologic causes, you should also consider appendicitis, cholecystitis, hepatitis, and pyelonephritis.

    Jeff: In the middle of that laundry list you mentioned there is one pathology which I think merits special attention - ovarian torsion. Don’t forget that patients undergoing ovarian stimulation as part of assisted reproductive technology are at a particularly increased risk due to the larger size of the ovaries.

    Nachi: Great point. Up next we have prehospital care...

    Jeff: Always a great section. First, prehospital providers should attempt to elicit an ob history. Including the number of weeks’ gestation, LMP, whether an IUP has already been confirmed, prior hx of ectopic, and a...


    Episode 23 - Influenza Diagnosis and Management in the Emergency Department Dec 01, 2018
    Show notes

    Jeff: Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, we’re talking about a topic that is ripe for review this time of year. We’re talking Influenza… Diagnosis and Management.

    Nachi: Very appropriate as the cold is settling in here in NYC and we’re already starting to see more cases of influenza. Remember that as you listen through the episode, the means we’re about to cover one of the CME questions for those of you listening at home with the print issue handy.

    Jeff: This month’s issue was authored by Dr. Al Giwa of the Icahn School of Medicine at Mount Sinai, Dr. Chinwe Ogedegbe of the Seton Hall School of Medicine, and Dr. Charles Murphy of Metrowest Medical Center.

    Nachi: And this issue was peer reviewed by Dr. Michael Abraham of the University of Maryland School of Medicine and by Dr. Dan Egan, Vice Chair of Education of the Department of Emergency Medicine at Columbia University.

    Jeff: The information contained in this article comes from articles found on pubmed, the cochrane database, center for disease control, and the world health organization. I’d say that’s a pretty reputable group of sources. Additionally, guidelines were reviewed from the american college of emergency physicians, infectious disease society of america, and the american academy of pediatrics.

    Nachi: Some brief history here to get us started -- did you know that in 1918/1919, during the influenza pandemic, about one third of the world’s population was infected with influenza?

    Jeff: That’s wild. How do they even know that?

    Nachi: Not sure, but also worth noting -- an estimated 50 million people died during that pandemic.

    Jeff: Clearly a deadly disease. Sadly, that wasn’t the last major outbreak… fifty years later the 1968 hong kong influenza pandemic, H3N2, took between 1 and 4 million lives.

    Nachi: And just last year we saw the 2017-2018 influenza epidemic with record-breaking ED visits. This was the deadliest season since 1976 with at least 80,000 deaths.

    Jeff: The reason for this is multifactorial. The combination of particularly mutagenic strains causing low vaccine effectiveness, along with decreased production of IV fluids and antiviral medication because of the hurricane, all played a role in last winter’s disastrous epidemic.

    Nachi: Overall we’re looking at a rise in influenza related deaths with over 30,000 deaths annually in the US attributed to influenza in recent years. The ED plays a key role in outbreaks, since containment relies on early and rapid identification and treatment.

    Jeff: In addition to the mortality you just cited, influenza also causes a tremendous strain on society. The CDC estimates that epidemics cost 10 billion dollars per year. They also estimate that an epidemic is responsible for 3 million hospitalized days and 31 million outpatient visits each year.

    Nachi: It is thought that up to 20% of the US population has been infected with influenza in the winter months, disproportionately hitting the young and elderly. Deaths from influenza have been increasing over the last 20 years, likely in part due to a growing elderly population.

    Jeff: And naturally, the deaths that we see from influenza also disproportionately affect the elderly, with up to 90% occurring in those 65 or older.

    Nachi: Though most of our listeners probably know the difference between an influenza epidemic and pandemic, let’s review it anyway. When the number of cases of influenza is higher than what would be expected in a region, an epidemic is declared. When the occurrence of disease is on a worldwide spectrum, the term pandemic is used.

    Jeff: I think that’s enough epidemiology for now. Let’s get started with the basics of the influenza virus. Influenza is spread primarily through direct person-to-person contact via expelled respiratory secretions. It is most active in the winter months, but can be seen year-round.

    Nachi: The influenza virus is a spherical RNA-based virus of the orthomyxoviridae family. The RNA core is associated with a nucleoprotein antigen. Variations of this antigen have led to the the 3 primary subgroups -- influenza A, B, and C, with influenza A being the most common.

    Jeff: Influenza B is less frequent, but is more frequently associated with epidemics. And Influenza C is the form least likely to infect humans -- it is also milder than both influenza A or B.

    Nachi: But back to Influenza A - it can be further classified based on its transmembrane or surface proteins, hemagglutinin and neuraminidase - or H and N for short. There are actually 16 different H subtypes and 9 different N subtypes, but only H1, H2, H3, and N1 and N2 have caused epidemic disease.

    Jeff: Two terms worth learning here are antigen drift and anitgen shift. Antigen drift refers to small point mutations to the viral genes that code for H and N. Antigen shift is a much more radical change, with reassortment of viral genes. When cells are infected by 2 or more strains, a new strain can emerge after genetic reassortment.

    Nachi: With antigen shift, some immunity may be maintained within a population infected by a similar subtype previously. With antigen drift, there is loss of immunity from prior infection.

    Jeff: The appearance of new strains of influenza typically involves an animal host, like pigs, horses, or birds. This is why you might be hear a strain called “swine flu”, “equine flu”, or “avian flu”. Close proximity with these animals facilitates co-infection and genetic reassortment.

    Nachi: I think that’s enough basic biology for now, let’s move on to pathophysiology. When inhaled, the influenza virus initially infects the epithelium of the upper respiratory tract and alveolar cells of the lower respiratory tract. Viral replication occurs within 4 to 6 hours. Incubation is 18 to 72 hours. Viral shedding is usually complete roughly 7 days after infection, but can be longer in children and immunocompromised patients.

    Jeff: As part of the infectious process and response, there can be significant changes to the respiratory tract with inflammation and epithelial cell necrosis. This can lead to viral pneumonia, and occasionally secondary bacterial pneumonia.

    Nachi: The secondary bacterial pathogens that are most common include Staph aureus, Strep pneumoniae, and H influenzae.

    Jeff: Despite anything you may read on the internet, vaccines work and luckily influenza happens to be a pathogen which we can vaccinate against. As such, there are 3 methods approved by the FDA for producing influenza vaccines -- egg-based, cell-based, or recombinant influenza vaccine. Once the season’s most likely strains have been determined, the virus is introduced into the medium and allowed to replicate. The antigen is then purified and used to make an injection or nasal spray.

    Nachi: It isn’t easy to create vaccines for all strains. H3N2, for example, is particularly virulent, volatile, and mutagenic, which leads to poor prophylaxis against this particular subgroup.

    Jeff: In fact, a meta-analysis on vaccine effectiveness from 2004-2015 found that the pooled effectiveness against influenza B was 54%, against the H1N1 pandemic in 2009 was 61%, and against the H3N2 virus was 33%. Not surprisingly, H3N2 dominant seasons are currently associated with the highest rates of influenza cases, hospitalizations, and death.

    Nachi: Those are overall some low percentages. So should we still be getting vaccinated? The answer is certainly a resounding YES.. Despite poor protection from certain strains, vaccine effectiveness is still around 50% and prevents severe morbidity and mortality in those patients.

    Jeff: That’s right. The 2017-2018 vaccine was only 40% effective, but this still translates to 40% less severe cases and a subsequent decrease in hospitalizations and death.

    Nachi: But before we get into actual hospitalization, treatment, and preventing death, let’s talk about the differential. We’re not just focusing on influenza here, but any influenza like illness, since they can be hard to distinguish. The CDC defines “influenza-like illness” as a temperature > 100 F, plus cough or sore throat, in the absence of a known cause other than influenza.


    Episode 22 - Electrical Injuries in the Emergency Department An Evidence-Based Review Nov 01, 2018
    Show notes

    Jeff: Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, we’re back with our old routine – no special guests.

    Nachi: Don’t sound so sad about it! Jeremy was great last month, and he’s definitely paved the way for more special guests in upcoming episodes.

    Jeff: You’re right. But this month’s episode is special in its own way - we’ll be tackling Electrical Injuries in the emergency department - from low and high voltage injuries to the more extreme and rare lightning related injuries.

    Nachi: And this is obviously not something we see that often, so listen up for some easy to remember high yield points to help you when you get an electrical injury in the ED. And pay particular attention to the , which, as always, signals the answer to one of our CME questions.

    Jeff: I hate to digress so early and drop a cliché, “let’s start with a case…” but we, just a month ago, had a lightning strike induced cardiac arrest in Pittsburgh, so this hits really close to home. Thankfully, that gentleman was successfully resuscitated despite no bystander CPR, and if you listen carefully, we hope to arm you with the tools to do so similarly.

    Nachi: This month’s print issue was authored by Dr. Gentges and Dr. Schieche from the Oklahoma University School of Community Medicine. It was peer reviewed by Dr. O’Keefe and Dr. Silverberg from Florida State University College of Medicine and Kings County Hospital, respectively.

    Jeff: And unlike past issues covering more common pathologies, like, say, sepsis, this month’s team reviewed much more literature than just the past 10 years. In total, they pulled references from 1966 until 2018. Their search yielded 477 articles, which was narrowed to 88 after initial review.

    Nachi: Each year, in the US, approximately 10,000 patients present with electrical burns or shocks. Thankfully, fatalities are declining, with just 565 in 2015. On average, between 25 and 50 of the yearly fatalities can be attributed to lightning strikes.

    Jeff: Interestingly, most of the decrease in fatalities is due to improvements in occupational protections and not due so much to changes in healthcare.

    Nachi: That is interesting and great to hear for workers. Also, worth noting is the trimodal distribution of patients with electrical injuries: with young children being affected by household currents, adolescent males engaging in high risk behaviors, and adult males with occupational exposures and hazards.

    Jeff: Electrical injuries and snake bites – leave it to us men to excel at all the wrong things… Anyway, before we get into the medicine, we unfortunately need to cover some basic physics. I know, it might seem painful, but it’s necessary. There are a couple of terms we need to define to help us understand the pathologies we’ll be discussing. Those terms are: current, amperes, voltage, and resistance.

    Nachi: So, the current is the total amount of electrons moving down a gradient over time, and it’s measured in amperes.

    Jeff: Voltage, on the other hand, is the potential difference between the top and bottom of a gradient. The current is directly proportional to the voltage. It can be alternating, AC, or direct, DC.

    Nachi: Resistance is the obstruction of electrical flow and it is inversely proportional to the current. Think of Ohm’s Law here. Voltage = current x resistance.

    Jeff: Damage to the tissues from electricity is largely due to thermal injury, which depends on the tissue resistance, voltage, amperage, type of circuit, and the duration of contact.

    Nachi: That brings us to an interesting concept – the let-go threshold. Since electrical injuries are often due to grasping an electric source, this can induce tetanic muscle contractions and therefore the inability to let go, thus increasing the duration of contact and extent of injury.

    Jeff: Definitely adding insult to injury right there. With respect to the tissue resistance, that amount varies widely depending on the type of tissue. Dry skin has high resistance, far greater than wet or lacerated skin. And the skin’s resistance breaks down as it absorbs more energy. Nerve tissue has the least resistance and can be damaged by even low voltage without cutaneous manifestations. Bone and fat have the highest resistance. In between nerve and bone or fat, we have blood and vascular tissue, which have low resistance, and muscle and the viscera which have a slightly higher resistance.

    Nachi: Understanding the resistances will help you anticipate the types of injuries you are treating, since current will tend to follow the path of least resistance. In high resistance tissues, most of the energy is lost as heat, causing coagulation necrosis. These concepts also explain why you may have deeper injuries beyond what can be visualized on the surface.

    Jeff: And not only does the resistance play a role, but so too does the amount and type of current. AC, which is often found in standard home and office settings, but can also be found in high voltage transmission lines, usually affects the electrically sensitive tissues like nerve and muscle. DC has a higher let-go threshold and does not cause as much sensation. It also requires more amperage to cause v-fib. DC is often found in batteries, car and computer electrical systems, some high voltage transmission lines, and capacitors.

    Nachi: Voltage has a twofold effect on tissues. The first mechanism is through electroporation, which is direct damage to cell membranes by high voltage. The second is by overcoming the resistance of body tissues and intervening objects such as clothes or water. You’re probably familiar with this concept when you see high voltages arcing through the air without direct contact with the actual electrical source, leading to diffuse burns.

    Jeff: As voltage increases, the resistance of dry skin is -- not surprisingly -- reduced, leading to worse injuries.

    Nachi: And for this reason, the US Department of Energy has set 600 Volts as the cutoff for low vs high voltage electrical exposure.

    Jeff: It is absolutely critical that we also mention and then re-mention throughout this episode, that those with electrical injuries often have multisystem injuries due to not only the thermal injury, electrical damage to electrically sensitive tissue, but also mechanical trauma. Injuries are not uncommon both from forceful pulling away from the source or a subsequent fall if one occurs.

    Nachi: That’s a great point which we’ll return to soon, as it plays an important role in destination selection. But before we get there, let’s review the common clinical manifestations of electrical injuries.

    Jeff: First up is – the cutaneous injuries. Most electrical injuries present with burns to the skin. Low voltage exposures typically cause superficial burns at the entry and exit sites, whereas high voltage exposures cause larger, deeper burns that may require skin grafting, debridement, and even amputation.

    Nachi: High voltage injuries can also travel through the sub-q tissue leading to extensive burns to deep structures despite what appears to be relatively uninjured skin. In addition, high voltage injuries can also result in superficial burns to large areas secondary to flash injury.

    Jeff: Electrical injuries can also lead to musculoskeletal injuries via either thermal or mechanical means. Thermal injury can lead to muscle breakdown, rhabdo, myonecrosis, edema, and in worse cases, compartment syndrome. In the bones, it can lead to osteonecrosis and periosteal burns.

    Nachi: In terms of mechanical injury – electrical injury often leads to forceful muscular contraction and falls. In 2 retrospective studies, 11% of patients with high voltage exposures also had traumatic injuries.

    Jeff: While not nearly as common, the rarer cardiovascular injuries are certainly up there as the most feared. Pay attention to the entry and exit sites, as the pathway of the shock is predictive of the potential for myocardial injury and arrhythmia. Common arrhythmias include AV block, bundle branch blocks, a fib, QT prolongation and even ventricular arrhythmias, including both v-fib and v-tach, both of which typically occur immediately after the injury.

    Nachi: There is a school of thought out there that victims of electrical injury can have delayed onset arrhythmias and require prolonged car


    Episode 21- Updates and Controversies in the Early Management of Sepsis and Septic Shock Oct 01, 2018
    Show notes

    Disclaimer: This is the unedited transcript of the podcast. Please excuse any typos.

    Jeff: Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, we’ll be talking Updates and Controversies in the Early Management of Sepsis and Septic Shock. We have a special episode for you this month… We’ve brought Dr. Jeremy Rose, one of the peer reviewers, and a sepsis expert, on with us to talk through the content this month.

    Jeremy: Dr. Jeremy Rose here. Thanks for having me in on this conversation. I’m always happy to talk about this topic because it’s clearly important. There’s a great deal of confusion around sepsis and I hope that in the next couple minutes we can clarify things in a way that really help your average front line doc trying to get it right.

    Nachi: So Dr. Rose, before we get started, tell us a bit about your background and your interest in sepsis…

    Jeremy: I’m the Assistant Medical Director and Sepsis Chair at Mount Sinai Beth Israel in Manhattan. For those listening, my hospital probably looks a little bit like yours. We’re busy, interesting, and just a little rough around the edges. We like it that way. More importantly, though, we mirror the national averages regarding sepsis. Roughly half of in-hospital mortality is associated with septic in some fashion. Pretty incredible when you think about it. Half.

    Jeff: Sepsis chair... clearly this is an important topic if it warrants it’s own chair at a major hospital in NYC. But getting back to the article this month. This month’s issue was authored by Faheem Guirgis, Laurent Page Black, and Elizabeth DeVos of the University of Florida, Department of Emergency Medicine.

    Nachi: And it was peer reviewed by Michael Allison, Assistant Director of the Adult ICU at Saint Agnes Hospital, and Jeremy Rose and Eric Steinberg of Mount Sinai Beth Israel.

    Jeff: So as well all know Sepsis is bread and butter emergency medicine, but, what is sepsis? It seems that every month or so we have a new guideline, bundle, definition, or whatever… I think it’s best to start with the basics - At its core, sepsis is a dysregulated response to infection that can be life-threatening.

    Nachi: Right and it’s the combined inflammatory with immunosuppressive features of sepsis that lead to the devastating organ dysfunction and even death. Optimal management of septic patients has been a source of intense research, stemming from the landmark study by Rivers in 2001. Jeremy, can you give us a little historical context there?

    Jeremy: Rivers was a real pioneer. He found a 16% mortality reduction with randomization to an early aggressive care bundle. Amazing work. That being said, many components of that bundle have since been disregarded. For example, Manny Rivers would measure CVP in all of his patients, something we rarely do.

    Nachi: Not to cut you off and steal your thunder there, but we’ll get to the most recent updates in management shortly. Let’s first talk definitions and terminology, and specifically, diagnosis, which is definitely a big elephant in the room. As Jeff mentioned a few minutes ago, diagnostic criteria have undergone so so so many changes.

    Jeff: Yes it has! 1991 marked the first standardized definition. Then in 2001, sepsis-2 was introduced. In 2014, the Society of Critical Care Medicine and the European Society of Intensive Care Medicine started a task force, and by 2016, updated definitions were out again! Sepsis-3!! A lot of this came after the realization that SIRS was just too broad and was overly sensitive and non-specific. Jeremy, why don’t you take us through Sepsis 3.

    Jeremy: So just to back up a little and frame this:

    Here’s the fundamental problem: As we likes to say, “there’s no troponin for sepsis.” And if you look at our patients, we tend not to miss the hypotensive, tachycardic, febrile patient. We know they’re septic. But how do we find the ones who don’t look as sick. Frequently elderly, possibly with normal-ish vitals and no fever. Those can be a lot harder to spot, but they may indeed be septic. Also, for research purposes we have to have a common definition, so Sepsis 3 came up with something called the SOFA score.

    The problem with the SOFA score is that its difficult to perform in the ED. It has parameters like bilirubin that often aren’t available when we want to screen out very sick patients. Fortunately there is the abridged version qSOFA, which identifies non-icu patients who are at high risk of inpatient mortality.

    So here it is, and if you get one thing from this episode, this is it:

    There are ONLY 3 criteria to the qSOFA. 3 Criteria. RR > 22; AMS; SBP <= 100. That’s it. If you have two of these criteria, you are up to 14 times more likely to die of sepsis during a hospital admission. That’s pretty profound; these patients are very sick. This is meant to replace SIRS. It also captures a much sicker population than the patients included in the Medicare definition.

    Jeff: So why do you think these parameters turn out to be so useful?

    Jeremy: Drilling down into these criteria you can see the pathophysiology at work. Obviously, SBP < 100 means sick. Interestingly, an elevated RR also turns out to be prognostic, because you’re seeing the compensation for an underlying acidosis. WHen you see a patient breathing quickly, it’s either from a primary respiratory problem or them trying to relieve an underlying acidosis. The caveat here is that you have to check it. At our hospital in southern Manhattan, patients tend to breathe around 16. At our hospital in northern Manhattan they like to breath around 18. It’s probably because the air is thinner. Seriously though, you have to actually measure RR for this to work. Temp is not in QSOFA but we should be checking that too. And I mean checking it by putting something that measures temperature inside the patient. We’ve looked at the forehead and tympanic thermometers and in real world conditions, they tend to underestimate by a degree or more. Think about that. A patient with a headache and a temperature of 99.5 is a very different patient than one with a temp of 100.5. Make sure you measure temperature.

    Nachi: Very true and these two patients can definitely go down very different management pathways! Rounding out our discussion on sepsis-3. We should note that severe sepsis is now a term of the past under Sepsis-3. And sepsis-3 redefined septic shock as “hypotension not responsive to fluid resuscitation” with the added requirement of vasopressors to maintain a MAP greater than or equal to 65 and with a lactate > 2. So quite a few changes!

    Jeff: And Jeremy, sticky topic coming up here. Center for Medicare and Medicaid Services (or CMS) quality measures - They haven’t really caught on to and adapted to Sepsis-3 yet, have they?

    Jeremy: The CMS mandate is based on the presence of SIRS criteria. Sepsis 3 is based on SOFA. This is definitely confusing. Part of the challenge in discussing this topic is separating out the QI guidelines from what is actually relevant to patient care based on the latest evidence-based medicine.

    Nachi: That seems fair. We’re really going to put you in an uncomfortable spot for a second and push you here Jeremy. Do you have any insight into why CMS isn’t interested in following the mountains of research that have led to sepsis-3? Is there a reason they are sticking to their current criteria?

    Jeremy: I think some of it is the slow pace of bureaucracy and the time that it takes to develop a consensus on management. Even if we can agree on who is septic, it’s really hard, if not impossible to link the care to a pay-for-performance metric which is what CMS ultimately would like to see. That’s not how Sepsis-3, or for that matter, SIRS, was designed to be used. You’re trying to take a tool which was originally designed for research and mold them into a tool used for pay for performance.

    Nachi: What a struggle. The CMS metrics are slightly different from the 2001 sepsis guidelines also. Take a look at Table 2 of the article for a quick comparison of sepsis-3, 2001 sepsis, and cms side-by-side. And for those on twitter, we’ll be sure to tweet this table out too for your review.

    Jeff: With so many different scores and definitions, I think that adequately sets the stage for the challenge this month’s authors faced coming up with real evidenced based guidelines.

    Nachi: Oh absolutely. And to make matters worse - this is a HUGE problem. We’re talking up to 850,000 ED visits annually in the US, and 19 million cases worldwide. Compounding this, sepsis results in death in approximately 1 out of 4 cases. Not only is it lethal, it is also very costly -- 17 billion dollars per year in the US alone!

    Jeff: And don’t forget importantly the 30-day hospital readmission rate. Sepsis is coming in at a higher readmission rate and cost per admission than acute MI, CHF, COPD, and PNA.

    Nachi: Let’s speak briefly on the etiology and pathophysiology of sepsis: we all know that sepsis is due to local infections that then become systemic. Previously, it was believed that the bacterial infection itself was the cause of the clinical syndrome of sepsis. However, we now know now that the syndrome of sepsis is due to the inflammatory and immunosuppressive mediators that were triggered by the infection. Normal immune regulatory safeguards fail and this leads to the syndrome. And interestingly, several studies have shown that critically ill septic patients experience reactivations of specific viruses that were previously limited to patients with severe immunosuppression.

    Jeff: Definitely something to look out for in your criticall...


    Episode 20 - Emergency Department Management of North American Snake Envenomations Sep 01, 2018
    Show notes

    Jeff: Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta and we’ll be taking you through the September 2018 issue of Emergency Medicine Practice - Emergency Department Management of North American Snake envenomations.

    Nachi: Although this isn’t something we encountered too frequently – it does seem like I’ve been hearing more about snake bites in the recent months.

    Jeff: I actually flew someone just the other day because the local ED ran out of CroFab after an envenomation in Western PA.

    Nachi: Yeah, this is definitely more than “just a boards topic,” and it’s really important to know about in those rare circumstances. In terms of incidence, there are actually about 10,000 ED visits in the US for snake bites each year, and 1/3 of these involve venomous species.

    Jeff: That’s a good teaser, so let’s start by recognizing this month’s team – the two authors, Dr. Sheikh, a medical toxicologist, and Patrick Leffers, a pharmD, and emergency medicine and clinical toxicology fellow. Both are at the University of Florida Jacksonville, and they reviewed a total of 120 articles from 2006-2017, in addition to reviews from both Cochrane and Dare.

    Nachi: And don’t forget our peer reviewers this month, Dr. Daniel Sessions, a medical toxicologist working at the South Texas Poison Center, and our very own editor-in-chief, Dr. Andy Jagoda, who is also Chair of the Department of Emergency Medicine at Mount Sinai in New York City.

    Jeff: What a team! But, let’s get back to the snakes. As some background, from 2006-2015 there were almost 66,000 reported snake exposures and 31 deaths from snake envenomation in the US. Of course, this number likely underestimates the true total.

    Nachi: And there are two key subfamilies of venomous snakes to be aware of – the Crotalinae – or pit vipers – which includes rattlesnakes, copperheads, and water moccasins; and the Elapidae – of which you really only need to know about the coral snake.

    Jeff: And while those are the only two NATIVE snake subfamilies to be acutely aware of, don’t forget that exotic snakes, which are shockingly popular pets -- they can also cause significant morbidity and mortality.

    Nachi: Oh, and one other quick note before we get into the epidemiology – most of the recommendations this month come from expert opinion, as high quality RCTs are obviously difficult. In addition, many of the studies were based in other countries, where the snakes, the anti-venoms and their availability, and the general healthcare systems are different from those that most of us work in.

    Jeff: Unless we have listeners abroad? Do we have listeners in other countries?

    Nachi: Oh we definitely do... but we are going to be a bit biased towards US envenomation today. In any case, venomous snake bites occur most frequently in men aged 18 to 49 during warmer months with provoked bites occurring more frequently in the upper extremities and unprovoked bites in the lower extremities.

    Jeff: In one study of poison center data from the last decade, nearly half of all victims of snake bites were victims of unknown type snakes. However, of those that were known, copperheads were the most common, while rattlesnakes caused the most fatalities – 19 of 31 in this dataset.

    Nachi: In a separate study of snake bites in the early 2000s, 32% of exposures were from venomous snakes and 59% of those resulted in admission. That’s remarkably high.

    Jeff: Snake bite severity depends on several key factors: the amount of venom, the composition of the venom, the body size of the bite victim, the victim's clothing, the size of the bite, comorbid conditions, and the timing and quality of medical care the victim receives.

    Nachi: To be a bit more specific - First, the amount of venom will depend on the species of snake, with variations even occurring within the same species. Secondly, while there is a correlation between rattlesnake size and bite severity, there is much more at play. Some snakes can even vary the amount of venom based on threat risk – with defensive bites having different profiles than bites to strike prey.

    Jeff: I found it pretty interesting that an estimated 10-25% of pit viper bites are considered dry bites, that is, ones in which no venom is released.

    Nachi: Right, this is just one reason why all victims shouldn’t immediately get anti-venom, but we’ll get there.

    Jeff: We definitely will. As we already stated – venom composition varies greatly. Pit vipers produce a predominantly hemotoxic venom. Systemic effects include tachycardia, tachypnea, hypotension, nausea, vomiting, weakness, and diaphoresis. Neurotoxicity is rare and is usually due to inter-breeding between species.

    Nachi: While rattlesnake bites are associated with higher morbidity and mortality, the more common copperhead bites typically only cause local tissue effects. More serious systemic findings such as coagulopathy and respiratory failure have been reported though.

    Jeff: So that’s a solid background to get us started. Let’s talk about the individual snakes. Why don’t you start with the crotalinae family – aka the pit vipers.

    Nachi: Sure – the crotalinae includes rattlesnakes, cottonmouths (also known as water moccasins), and copperheads. These make up the vast majority of reports to the poison centers. They can be identified by their heat sensing pits located behind their nostrils (hence pit vipers). As a general rule, you can also identify the venomous snakes by their triangular or spade-like head, elliptical pupils, and hollow retractable fangs.

    Jeff: wait, so you want me to walk up to the snake and ask to see if their fangs retract… yea, no thanks.

    Nachi: Haha, of course not, I’m just giving you some of the general principles here. In contrast, non-venomous pit vipers have rounded heads, round pupils, a double row of vertical scales, and they lack fangs.

    Jeff: In terms of location, rattlesnakes are found in all states but Hawaii, and cottonmouths and copperheads are distributed mostly throughout the southern and southeastern states, with copperheads also extending further north, even into Massachusetts.

    Nachi: Moving on to the Elapidae – there are 3 species of coral snakes, only two of which you need to know about, Micrurus fulvius fulvius or the eastern coral snake and Micrurus tener or the Texas coral snake. Of the two, the eastern or Micrurus fulvius fulvius produces more potent venom.

    Jeff: As you may have guessed by their names, the eastern coral snake is found in the southeastern united states, specifically, east of the Mississippi -- whereas the Texas coral snake lives west of the Mississippi.

    Nachi: Venomous North American coral snakes can be recognized by the red and yellow bands around their bodies whereas their nonvenomous counterparts can be recognized by their characteristic black band between the red and yellow bands. I’m sure you’ve heard the popular mnemonic for this… Red touch yellow kill a fellow, red touch black, venom lack.

    Jeff: I have heard that one, and it’s not a bad mnemonic. Just remember that this is more of a guideline than a rule, as it doesn’t always hold true.

    Nachi: Coral snakes also tend to chew rather than bite thanks to their short, fixed, hollow fangs. Locally, bites can lead to muscle destruction thanks to a certain myotoxin. Systemic signs of infection include nausea, vomiting, abdominal pain, and dizziness.

    Jeff: The venom also contains a neurotoxin which can lead to diplopia, difficulty swallowing and speaking and generalized weakness.

    Nachi: Complicating matters even further, the onset of these symptoms may be delayed for many hours.

    Jeff: Alright, so I think that about wraps up the background. Let’s move on to the meat and potatoes of this article, starting with the differential.

    Nachi: For differential this month, we are really focusing on differentiating a venomous snake from a non-venomous one.

    Jeff: Oh yeah, this is where you want us to ask the snake if it can retract its fangs, right?

    Nachi: Ha very funny – Although the type of snake may be obvious if the patient...


    Episode 19 - Cannabinoids: Emerging Evidence in Use and Abuse Aug 01, 2018
    Show notes

    Show Notes

    Disclaimer: This is the unedited transcript of the podcast. Please excuse any typos.

    Jeff: Welcome back to Emplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta and we’ll be taking you through the August 2018 issue of Emergency Medicine Practice.

    Nachi: This month’s topic is one that Jeff has significant personal experience with from his college days. We’re reviewing Cannabinoids -- and emerging evidence in their use and abuse.

    Jeff: Um… that is definitely not true. I was actually a varsity rower in college... Are we still reviewing talking points together before we start recording these episodes?

    Nachi: Sometimes…

    Jeff: This month’s issue was authored by Mollie Williams, who is the EM residency program director at the Brooklyn Hospital Center. It was peer-reviewed by Joseph Habboushe, assistant professor at NYU and Nadia Maria Shaukat, director of the emergency and critical care ultrasound at Coney Island Hospital in Brooklyn, New York.

    Nachi: We’re going to be talking about the pathophysiology of cannabinoids, clinical findings in abuse, best practice management, differences between natural and synthetic cannabinoids, and treatment for cannabinoid hyperemesis syndrome. So buckle up and get ready.

    Jeff: As you’re listening through this episode, remember that the means that we are about to answer one of the CME questions from the end of the print issue. If you’re not driving while listening, be sure to jot down these answers and get your CME credit when we’re going through this issue..

    Nachi: As of June 2018, there are 31 states, the District of Columbia, and 2 US territories that possess state and local-level laws allowing the use of cannabis medicinally or in recreational formulations. Marijuana actually maintains the highest lifetime use of an illicit drug used within the US.

    Jeff: There are a shocking 22 million past-month users of marijuana in the US, followed by pain relievers at 3.8 million, and cocaine at 1.9 million. Clearly, an important topic worth discussion, especially as synthetic products have become more widely available.

    Nachi: And worth noting -- Colorado, where medicinal and recreational marijuana use has been decriminalized and later legalized, has shown a nearly 2-fold increase in the prevalence of ED visits, which may be related to marijuana exposure.

    Jeff: Medicinally, cannabinoids are currently used in the treatment of chronic pain syndromes, complications of multiple sclerosis and paraplegia, weight loss due to appetite suppression in HIV/aids, chemotherapy-induced nausea and vomiting, seizures, and many other neuropsychiatric disorders. In fact, cannabis use has been documented for medical use dating as far back as 600 BC in West and Central Asia.

    Nachi: All of that being said though, there is an absence of high-quality reviews and evidence to support the use of cannabinoids for any of the indications you just mentioned. And the US DEA maintains cannabis as a Schedule I substance.

    Jeff: This DEA designation limits the ability to do research and obtain federal funding for such research. General lack of federal regulations on chemical content also leads to product variation, which may be a cause of increased incidences of accidental overdoses.

    Nachi: To attain the most up to date information for this article, Dr. Williams searched the PubMed and Cochrane Databases from 1950 to 2018. This produced predominantly case reports and retrospective studies. There were just a few randomized prospective studies -- not surprising.

    Jeff: Let’s get started with the pathophysiology. There are 3 cannabis species to be aware of: Cannabis sativa, cannabis indica, and cannabis ruderalis. Within these species, over 545 active cannabis-derived components have been described.

    Nachi: There are ten main constituents of cannabis sativa. Of these, 9-tetrahydrocannabinol (delta-9-THC) and cannabidiol (CBD) are found in the greatest quantities. The neuropsychiatric and addictive properties of cannabis are due primarily to the delta-9-THC.

    Jeff: THC and other cannabis derivatives work through the endocannabinoid system and other neuroregulators. The endogenous cannabinoid system has 4 components: (1) endogenous endocannabinoids, (2) receptors, (3) degradation enzymes, and (4) transport mechanisms.

    Nachi: There are two endogenous endocannabinoids to know about: anandamide (AEA) and 2-arachidonoyl-glycerol.

    Jeff: Cannabinoid receptors are broadly dispersed through the central nervous system, and to a lesser degree, also to other organ systems.

    Nachi: Because CB receptors are concentrated within the central nervous system, they exert the majority of their effects on the neuropsychiatric systems. And -- yes that’s a double ding -- the cannabinoid 1 (or CB1) receptor is most responsible for cannabis-induced neuropsychiatric effects.

    Jeff: Interestingly, the anti-emetic effects and possible palliative properties of cannabis derivatives are thought to be secondary to the inhibitory effects on serotonin receptors and the excitatory effects on the transient receptor potential vanilloid 1 (or TRPV1). More on TRPV1 later...

    Nachi: So far we have been talking about cannabinoids from the cannabis plant, but with cannabis being illegal in many states, there has been a growing emergence of synthetic cannabinoids. Synthetics were initially developed in the 1980s largely for research purposes.

    Jeff: Because the current DEA controlled substances schedule designations are based on original chemical names, synthetics have gained popularity as manufacturers are able to produce newer compounds and circumvent DEA designation as well as routine urine drug screening tests.

    Nachi: You may be familiar with some of the street names for synthetics -- like spice, K2, scooby snacks, black mamba, kush, and kronic. These can often be purchased over the internet or through specialty smoke shops.

    Jeff: Scooby Snacks, what a fantastic name, mooovingggg on… Synthetic cannabinoids often have greater affinity for the CB1 receptor than naturally occurring cannabinoids -- and synthetics can produce 100 times the effect. As a result, the presenting symptoms with synthetic intoxication can be difficult to differentiate from crystal meth or bath salt abuse.

    Nachi: Manufacturers sometimes use solvents and other contaminants. Clusters of toxic ingestions and deaths have occurred. Emergency clinicians need to be aware of this and should report suspicious events immediately.

    Jeff: For more on synthetic intoxications in the ED, be sure to take a look at the recent May 2018 issue of Pediatric Emergency Medicine Practice on Synthetic Drug Intoxication in Children if you haven’t already read it. Also, just a quick FYI - If you’re not a current subscriber to Pediatric Emergency Medicine Practice, we’re giving away a free copy of the issue specifically for our listeners. Just head over to ebmedicine.net/drugs for the PDF of the issue.

    Nachi: A free issue for our listeners, that’s nice! Let’s move on to a discussion about current indications for cannabinoids. So, there is no clear consensus on these indications, but there is some research of varying quality that supports the treatment of some chronically debilitating diseases with cannabinoids.

    Jeff: A systematic review and meta-analysis from 2015 found low-quality evidence to support cannabis therapy for appetite suppression in HIV and aids patients; moderate-quality evidence for treatment of chronic pain and spasticity; and also moderate quality evidence for some chronic debilitating diseases.

    Nachi: While talking about evidence-based medicine here, another review by the National Academies of Science, Engineering, and Medicine on possible associations between cannabis and cancers arising in the lungs, head, and neck, or testicles -- showed no statistically significant associations exist.

    Jeff: So in case that wasn’t clear - the overall evidence to support cannabis therapy, in general, is weak. Also, be aware that there are various formulations of cannabis that allow for different routes of administration. We’re talking oils, tinctures, teas, extracts, edibles like candies and baked goods, parenteral formulations, eye solutions, intranasal, sublingual, transmucosal, tablets, sprays, skin patches, topical creams, rectal suppositories, and capsules -- just to name, a few.

    Nachi: A few! That seems pretty complete to me. Basically, any way you can imagine, it seems like a route of administration has been explored. But of importance, these formulations have different absorption times -- as you might expect. The shortest duration to peak plasma levels of delta-9-THC is through the inhalation route, which can produce effects within 3 minutes. On the longer end, rectal cannabis administration can take up to 8 hours to reach peak plasma concentrations.

    Jeff: Let’s talk about some of the clinical findings and systemic effects associated with cannabis use. First up is the link between cannabis use and stroke or TIA. Cannabis users wh...


    Episode 18 – Emergency Department Management of Dyspnea in the Dying Patient Jul 01, 2018
    Show notes

    Join Jeff, a former firefighter, and Nachi, a former mathematician, as they take you through the July 2018 issue of Emergency Medicine Practice: Emergency department management of dyspnea in the dying patient

    Most Important References

    17. Reuben DB, Mor V. Dyspnea in terminally ill cancer patients. Chest. 1986;89(2):234-236. (Prospective; 1754 patients)34. Lunney JR, Lynn J, Foley DJ, et al. Patterns of functional decline at the end of life. JAMA. 2003;289(18):2387-2392. (Prospective cohort; 4190 patients)40. Steinhauser KE, Christakis NA, Clipp EC, et al. Factors considered important at the end of life by patients, family, physicians, and other care providers. JAMA. 2000;284(19):2476-2482. (Cross-sectional survey; 1122 patients/families/providers)41. Quill TE, Arnold R, Back AL. Discussing treatment preferences with patients who want “everything.” Ann Intern Med. 2009;151(5):345-349. (Review)63. Clemens KE, Quednau I, Klaschik E. Use of oxygen and opioids in the palliation of dyspnoea in hypoxic and non-hypoxic palliative care patients: a prospective study. Support Care Cancer. 2009;17(4):367-377. (Nonrandomized trial; 46 patients)66. Abernethy AP, McDonald CF, Frith PA, et al. Effect of palliative oxygen versus room air in relief of breathlessness in patients with refractory dyspnoea: a double-blind, randomised controlled trial. Lancet. 2010;376(9743):784-793. (Double-blind randomized controlled trial; 239 patients)68. Galbraith S, Fagan P, Perkins P, et al. Does the use of a handheld fan improve chronic dyspnea? A randomized, controlled, crossover trial. J Pain Symptom Manage. 2010;39(5):831-838. (Randomized controlled crossover trial; 50 patients)

    Episode 17 - Managing Shoulder Injuries in the Emergency Department Fracture, Dislocation, and Overuse Jun 01, 2018
    Show notes

    Join hosts Jeff Nusbaum, MD, and Nachi Gupta, MD on this episode of EMplify as they take you through the June 2018 issue of Emergency Medicine Practice: Managing Shoulder Injuries in the Emergency Department Fracture, Dislocation, and Overuse. This month, Richard Pescatore, director of clinical research at Crozer-Keystone Health System and clinical assistant professor at the Rowan University School of Osteopathic Medicine, along with Andrew Nyce, vice chairman and associate professor at cooper medical school of Rowan University reviewed just over 100 articles to come up with their evidence-based recommendations. Their recommendations were then edited by John Munyak of Maimonides and Mark Silverberg of SUNY Downstate and Kings County Hospital. Most Important References * Ponce BA, Kundukulam JA, Pflugner R, et al. Sternoclavicular joint surgery: how far does danger lurk below? J Shoulder Elbow Surg. 2013;22(7):993-999. (Prospective cohort; 49 patients) * Slaven EJ, Mathers J. Differential diagnosis of shoulder and cervical pain: a case report. J Man Manip Ther. 2010;18(4):191-196. (Case report) * Helfen T, Ockert B, Pozder P, et al. Management of prehospital shoulder dislocation: feasibility and need of reduction. Eur J Trauma Emerg Surg. 2016;42(3):357-362. (Retrospective review; 70 patients) * Lenza M, Belloti JC, Andriolo RB, et al. Conservative interventions for treating middle third clavicle fractures in adolescents and adults. Cochrane Database Syst Rev. 2014(5):CD007121. (Systematic review; 3 trials, 354 patients) * Neer CS, 2nd. Displaced proximal humeral fractures: part I. Classification and evaluation. 1970. Clin Orthop Relat Res. 2006;442:77-82. (Review article) * Sholsberg J, Jackson R. Best evidence topic report. Intra-articular corticosteroid injections in acute rheumatoid monoarthritides. Emerg Med J. 2004;21(2):204. (Systematic review; 1 study, 137 patients)


    Episode 16 - Recognizing and Managing Emerging Infectious Diseases in the Emergency Department May 01, 2018
    Show notes

    Join hosts Jeff Nusbaum, MD, and Nachi Gupta, MD on this episode of EMplify as they take you through the May 2018 issue of Emergency Medicine Practice: Recognizing and Managing Emerging Infectious Diseases in the Emergency Department. This month’s issue was authored by Drs. Millan, Thomas-Paulose, and Egan from Mount Sinai St Luke’s and Mount Sinai West in New York city.


    Episode 15 - Jaundice in the Emergency Department: Meeting the Challenges of Diagnosis and Treatment Apr 01, 2018
    Show notes

    Jaundice is a manifestation of elevated serum bilirubin, and can have many causes, some of which can be life-threatening. Join hosts Jeff Nusbaum, MD, and Nachi Gupta, MD on this episode of EMplify as they take you through the April 2018 issue of Emergency Medicine Practice: Jaundice in the Emergency Department: Meeting the Challenges of Diagnosis and Treatment. This month’s issue was authored by Dr. Taylor and Dr. Wheatley both of the Emory School of Medicine. It was peer reviewed by Dr. Chung of the Icahn School of Medicine at Mount Sinai, and Dr. Horan of Our Lady of Lourdes Medical Center.


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