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, after a few months of primarily medical topics, we’re talking trauma, specifically Blunt Cardiac Injury: Emergency Department Diagnosis and Management.

Nachi: With no gold standard diagnostic test and with complications ranging from simple ectopic beats to fulminant cardiac failure and death, this isn’t an episode you’ll want to miss.

Jeff: Before we begin, let me give a quick shout out to our incredible group of authors from New York -- Dr. Eric Morley, Dr. Bryan English, and Dr. David Cohen of Stony Brook Medicine and Dr. William Paolo, residency program director at SUNY Upstate. I should also mention their peer reviewers Drs. Jennifer Maccagnano and Ashley Norse of the NY institute of technology college of osteopathic medicine and UF Health Jacksonville, respectively.

Nachi: This month’s team parsed through roughly 1200 articles as well as guidelines from the eastern association for surgery in trauma also known as EAST.

Jeff: Clearly a large undertaking for a difficult topic to come up with solid evidence based recommendations.

Nachi: For sure. Let’s begin with some epidemiology, which is admittedly quite difficult without universally accepted diagnostic criteria.

Jeff: As you likely know, despite advances in motor vehicle safety, trauma remains a leading cause of death for young adults. In the US alone, each year, there are about 900,000 cases of cardiac injury secondary to trauma. Most of these occur in the setting of vehicular trauma.

Nachi: And keep in mind, that those injuries don’t occur in isolation as 70-80% of patients with blunt cardiac injury sustain other injuries. This idea of concomitant trauma will be a major theme in today’s episode.

Jeff: It certainly will. But before we get there, we have some more definitions to review - cardiac concussion and contusion, both of which were defined in a 1989 study. In this study, cardiac concussion was defined as an elevated CKMB with a normal echo, while a cardiac contusion was defined as an elevated CKMB and abnormal echo.

Nachi: Much to my surprise, though, abnormal echo and elevated ck-mb have not been shown to be predictive of adverse outcomes, but conduction abnormalities on ekgs have been predictive of development of serious dysrhythmia

Jeff: More on complications in a bit, but first, returning to the idea of concomitant injuries, in one autopsy study of nearly 1600 patients with blunt trauma - cardiac injuries were reported in 11.9% of cases and contributed to the death of 45.2% of those patients.

Nachi: Looking more broadly at the data, according to one retrospective review, blunt cardiac injury may carry a mortality of up to 44%.

Jeff: That’s scary high, though I guess not terribly surprising, given that we are discussing heart injuries due to major trauma...

Nachi: The force may be direct or indirect, involve rapid deceleration, be bidirectional, compressive, concussive, or even involve a combination of these. In general, the right ventricle is the most frequently injured area due to the proximity to the chest wall.

Jeff: Perfect, so that's enough background, let’s talk differential. As you likely expected, the differential is broad and includes cardiovascular injuries, pulmonary injuries, and other mediastinal injuries like pneumomediastinum and esophageal injuries.

Nachi: Among the most devastating injuries on the differential is cardiac wall rupture, which not surprisingly has an extremely high mortality rate. In terms of location of rupture, both ventricles are far more likely to rupture than the atria with the right atria being more likely to rupture than the left atria. Atrial ruptures are more survivable, whereas complete free wall rupture is nearly universally fatal.

Jeff: Septal injuries are also on the ddx. Septal injuries occur immediately, either from direct impact or when the heart becomes compressed between the sternum and the spine. Delayed rupture can occur secondary to an inflammatory reaction. This is more likely in patients with a prior healed or repaired septal defects.

Nachi: Valvular injuries, like septal injuries, are rare. Left sided valvular damage is more common and carries a higher mortality risk. In order, the aortic valve is more commonly injured followed by the mitral valve then tricuspid valve, and finally the pulmonic valve. Remember that valvular damage can be due to papillary muscle rupture or damage to the chordae tendineae. Consider valvular injury in any patient who appears to be in cardiogenic shock, has hypotension without obvious hemorrhage, or has pulmonary edema.

Jeff: Next on the ddx are coronary artery injuries, which include lacerations, dissections, aneurysms, thrombosis, and even MI secondary to increased sympathetic activity and platelet activity after trauma. In one review, dissection was the most commonly uncovered pathology, occurring 71% of the time, followed by thrombosis, which occured only 7% of the time. The LAD is the most commonly injured artery followed by the RCA.

Nachi: Pericardial injury, including pericarditis, effusion, tamponade, and rarely rupture, is also certainly on the differential.

Jeff: In terms of dysrhythmias, sinus tachycardia is the most common dysrhythmia, with other rhythms, including PVC / PAC / and afib being found only 1-6% of the time.

Nachi: And while conduction blocks are rare, a RBBB is the most commonly noted, followed by a 1st degree AVB.

Jeff: Though also rare, commotio cordis deserves it’s own section as its the second most common cause of death in athletes < 18 who are victims of blunt trauma. Though only studied in swine models, it’s hypothesized that the impact to the chest wall during T-wave upstroke can precipitate v-fib.

Nachi: Aortic root injuries usually occur at the insertion of the ligamentum arteriosum and isthmus. Such injuries typically result in aortic insufficiency.

Jeff: And the last pathology on the differential requiring special attention is a myocardial contusion. Again, no standard definition exists, with some diagnostic criteria including simply chest pain and increasing cardiac enzymes, and others including cardiac dysfunction, ecg abnormalities, wall motion abnormalities, and an elevation of cardiac enzymes.

Nachi: Certainly a pretty broad differential… before moving on to the work up, Jeff why don’t you get us started with prehospital care?

Jeff: Prehospital management should focus on rapid identification and stabilization of life threatening injuries with expeditious transport as longer prehospital times have been associated with increased mortality in trauma. Immediate transport to a Level I trauma center should be the highest priority for those with suspected blunt cardiac injury.

Nachi: In terms of who specifically should be transporting the patient, a Cochrane review evaluated the utility of ALS vs BLS transport in trauma. There is reasonably good data to support BLS over ALS, even when controlling for trauma severity. Moreover, when airway management is needed, advanced airway techniques by ALS crews were associated with decreased odds of survival. Regardless of who is there, the message is the same: focus not on interventions, but instead on rapid transport.

Jeff: And if it does happen to be an ALS transport crew, without delaying transport, pain management with fentanyl is both safe and reasonable and preferred over morphine. Post opiate hypotension in prehospital trauma patients is a rare but documented complication.

Nachi: And if the prehospital team is lucky enough, or maybe unlucky enough, i don’t know, to have a credentialed provider who can perform ultrasound for those suspected of having a blunt cardiac injury, the general prehospital data on ultrasound is sparse. As of now, it’s difficult to conclude if prehospital US improves care for trauma patients.

Jeff: Interestingly, the system I work in has prehospital physicians, who do carry US, but I can’t think of a major trauma where ultrasound changed any of the decisions we made.

Nachi: Right, and I think that just reinforces the main point here: there may be a role, we just don’t have the data to support it at this time.

Jeff: Great, let’s move onto ED care, beginning with the H&P.

Nachi: On history, make sure to elucidate if there is any chest pain, and if it’s onset was before or after the traumatic event. In addition, make sure to ask about dyspnea, fatigue, palpitations, and lightheadedness.

Jeff: And don’t forget to get the crash details from the EMS crew before they depart! As a side note, for anyone taking oral boards in a few months, don’t forget to ask the EMS crew for the details!!!

Nachi: A definite must for oral boards and for your clinical practice.

Jeff: In terms of the physical, tachycardia is the most common abnormality in blunt cardiac injury. In those with severe injury, you may note refractory hypotension secondary to cardiogenic shock. But don’t be reassured by normal vitals, especially in the young, who may be compensating well despite being quite ill.

Nachi: Fully undress the patient to appropriately inspect and percuss the chest wall - looking for signs of previous cardiac surgeries or pacemaker placement, as well as to auscultate for new murmurs which may be a sign of valvular injury.

Jeff: Similarly, as concomitant injuries are common, inspect the abdomen, looking for ecchymosi...

Shownotes

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 tackling an incredibly important topic - evaluation and management of life threatening headaches in the Emergency Department.

Nachi: Fear not, this will not simply be “who needs a head CT episode”; we’ll cover much more than that. Listen closely as this is an important topic, with huge consequences for mismanagement.

Jeff: Absolutely. As some quick background - headaches account for 3% of all ED visits in the US, with 90% being benign primary headaches and less than 10% being secondary to other causes like vascular, infectious, or traumatic etiologies. It’s within these later 10% that we are looking for the red flag signs to identify the potentially life-threatening headaches.

Nachi: And to do so, Dr. David Zodda and Dr. Amit Gupta, PD and APD at Hackensack University Medical and Trauma Center, and their colleague Dr. Gabrielle Procopio, a PharmD, have done a fantastic job parsing through the literature, which included over 500 abstracts, 89 full text articles, guidelines from ACEP and the American Academy of Neurology, as well as canadian and european neurology guidelines, to summarize the best evidence based recommendations for you all.

Jeff: We would be remiss to not also mention Dr. Mert Erogul of Maimonides Medical Center and Dr. Steven Godwin, Chair of Emergency Medicine at the University of Florida College of Medicine.

Nachi: Alright, so let’s get started with some definitions and pathophysiology. The international classification of headache disorders 3, or ICHD-3, classifies headaches into primary, secondary, and cranial neuropathies.

Jeff: Primary headache disorders include migraine, tension, and cluster headaches. Secondary headaches include those secondary to vascular disorders, traumatic disorders, and disorders in hemostasis. These are the potentially life threatening headaches that can have a mortality has high as 50%.

Nachi: And the final category includes cranial neuropathies, such as trigeminal neuralgia.

Jeff: And I think we can safely say that that wraps up our discussion in this episode on cranial neuropathies, moving on….

Nachi: Headaches result from traction to or irritation of the meninges and blood vessels, which are the only innervated central nervous system structures. Activation of specific nerve ganglion complexes by neuropeptides like -- substance P and calcitonin gene-related peptide -- are thought to contribute to head pain.

Jeff: It is important to note that all headache pain shares common pain pathways, thus response to pain medications does not exclude potential life threatening secondary causes of headache. This led to the ACEP guideline which states just that..

Nachi: I feel like that deserves ding sound as it's a critically important point. To repeat, just because a pain medication relieves a headache, that does not exclude dangerous secondary causes!

Jeff: And what are the life threatening headaches? Life-threatening headaches include subarachnoid hemorrhage, cervical Artery Dissection, which includes both vertebral Artery Dissection and carotid artery dissection, cerebral Venous Thrombosis, idiopathic intracranial hypertension, giant cell arteritis, and posterior reversible encephalopathy syndrome, or PRES.

Nachi: Slow down for a second and let’s not skip over your favorite section.. Let’s talk pre hospital care for headache patients.

Jeff: Good call! Pre-hospital care is fairly straightforward and includes a primary survey, conducting a focused neurologic exam, and assessing for red flag signs, which include focal neurologic deficits, sudden onset headache, new headache in those over 50, neck pain or stiffness, changes in visual Acuity, fever or immunocompromised State, history of malignancy, pregnancy or postpartum status, syncope, and seizure. That’s quite a list. For a visual reference, see Table 3 in the print issue.

Nachi: And patients with neurologic deficits or severe sudden-onset headaches, should be transported immediately to the nearest available stroke center. Tylenol should be offered for pain management. Avoid opioids and nsaids.

Jeff: Upon arrival to the emergency department, history and physical should include your standard vitals, testing neurologic function, cranial nerve testing, head and neck exam, as well as a fundoscopic exam. As was the case for your pre-hospital colleagues, you should also assess for red flag signs for life-threatening headaches. Check out tables 2, 3, and 4 for more details here.

Nachi: With respect to Vital Signs, in the setting of an acute headache, severe hypertension should prompt a search for signs of end-organ damage such as hypertensive encephalopathy, intracranial Hemorrhage, PRES, and preeclampsia in pregnant women. Additionally, fever, and especially fever and neck stiffness, should raise concern for CNS infection.

Jeff: For your neurologic examination, make sure to include assessments of motor strength, coordination, reflexes, sensory function, and gait. Don't forget that lesions involving the anterior circulation, such as dysarthria, cognitive impairment, and Horner syndrome may be indicative of a carotid artery dissection, whereas dizziness, vision changes, and limb weakness may be due to a vertebral Artery Dissection.

Nachi: And for cranial nerve testing - pay particular attention to cranial nerves 2, 3 and 6. For cranial nerve 2 - look out for an afferent pupillary defect, or a marcus-gunn pupil, which is seen in optic neuritis, giant cell artertitis, and central retinal artery occlusion. For CN3, oculomotor nerve palsies raise concern for a posterior communicating aneurysm and SAH. And lastly, CN6 palsies, which often presents with diplopia on lateral gaze , are often seen with intracranial idiopathic hypertension and cerebral venous thrombosis, in addition to impaired visual acuity, visual field defects, and tunnel vision.

Jeff: For the head and neck exam, remember that a partial horner syndrome, with miosis and ptosis without anhidrosis, may be indicative of a cervical artery dissection. Unfortunately, if the patient presents acutely, their only complaint may be pain, as the neurologic sequelae may take days to develop.

Nachi: Additionally, with respect to the head and neck exam, evaluate the patient for tenderness and beading along the temporal artery.

Jeff: One review noted that temporal artery beading actually had the highest likelihood ratio for GCA, 4.6, whereas temporal artery tenderness only had a LR of 2.6

Nachi: And the last physical exam maneuver you should ideally perform is a fundoscopic exam for papilledema, which is often seen in IIH, malignant hypertension, and CVT.

Jeff: Perfect so that rounds out the physical, next we have diagnostic studies. Most importantly, routine lab testing is typically of low utility in aiding in the diagnosis of headache.

Nachi: Even ESR and CRP in the setting of possible giant cell arteritis have poor sensitivity and specificity to diagnose it. So even if the ESR and CRP are negative, if the suspicion for GCA is high enough, it should be treated and you should get a biopsy.

Jeff: Do consider adding on a venous or arterial carboxyhemoglobin in the right clinical scenario, as CO poisoning represents an important cause of headache you wouldn’t want to miss. This is especially important at this time of year when heating systems are working overtime here in the states.

Nachi: And hopefully you have a co-oximeter, so you can even check this non-invasively.

Jeff: Interestingly, there may be a unique role for a d-dimer here as well. Several small studies have used the d-dimer to risk stratify patients with possible CVT. In one study a d-dimer level < 500 mcg/L had a 97% sensitivity and a negative predictive value of 99% - not bad!

Nachi: Pretty impressive performance characteristics. I think that about wraps up lab work. Let’s talk radiology.

Jeff: Though low yield, CT utilization is estimated at 2.5-10% of non-traumatic headaches. A non-con CT should be reserved for those with suspicion for an intracranial hemorrhage, while a contrast CT would be required in those in whom there is concern for an infectious process or space occupying lesion.

Nachi: CT angio or MRI should be used in cases of possible cervical artery dissection. MRI also is the neuroimaging of choice for PRES, which is more sensitive for cerebral edema than CT.

Jeff: Similarly, MRV is recommended in those with a concerning story for CVT.

Nachi: To help guide your emergent neuroimaging utilization, ACEP suggests imaging in those with headache and an abnormal finding on neuro exam, those with new and sudden-onset severe headache, HIV positive patients with new headache, and those over 50 with a new headache.

Jeff: With that in mind, let’s dive a bit deeper into the use of CT for SAH, a topic which doesn’t get a ding sound, but is certainly critically important. Recent literature have found that a CT within 6 hours of symptom onset has a sensitivity and specificity and negative predictive value of 100%. In addition, one 2016 study demonstrated a LR of 0.01 in those with a negative HCT within 6 hours. These are really important results because that means SAH is essentially ruled out with a negative study.

Nachi: Unfortunately, the 2008 ACEP guideline and 2012 AHA guidelines still recommend a lumbar puncture in those being worked up for SAH. Luckily the ACEP guideline is currently being revised so your decision to forego the LP with a negative HCT in the fi

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...

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.

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