Podcasts about Etomidate

Contributor: Ricky Dhaliwal MD Educational Pearls:  Etomidate was previously the drug of choice for rapid sequence intubation (RSI) However, it carries a risk of adrenal insufficiency as an adverse effect through inhibition of mitochondrial 11-β-hydroxylase activity A recent meta-analysis analyzing etomidate as an induction agent showed the following: 11 randomized-controlled trials with 2704 patients Number needed to harm is 31; i.e. for every 31 patients that receive etomidate for induction, there is one death The probability of any mortality increase was 98.1% Ketamine is preferable due to a better adverse effect profile Laryngeal spasms and bronchorrhea are the most common adverse effects after IV push Beneficial effects on hemodynamics via catecholamine surge, albeit not as pronounced in shock patients 2023 meta-analysis compared ketamine and etomidate for RSI Ketamine's probability of reducing mortality is cited as 83.2% Overall, induction with ketamine demonstrates a reduced risk of mortality compared with etomidate The dosage of each medication for induction Etomidate: 20 mg based on 0.3 mg/kg for a 70 kg adult Ketamine: 1-2 mg/kg (or 0.5-1 mg/kg in patients with shock) Patients with asthma and/or COPD also benefit from ketamine induction due to putative bronchodilatory properties References  Goyal S, Agrawal A. Ketamine in status asthmaticus: A review. Indian J Crit Care Med. 2013;17(3):154-161. doi:10.4103/0972-5229.117048 Koroki T, Kotani Y, Yaguchi T, et al. Ketamine versus etomidate as an induction agent for tracheal intubation in critically ill adults: a Bayesian meta-analysis. Crit Care. 2024;28(1):1-9. doi:10.1186/s13054-024-04831-4 Kotani Y, Piersanti G, Maiucci G, et al. Etomidate as an induction agent for endotracheal intubation in critically ill patients: A meta-analysis of randomized trials. J Crit Care. 2023;77(April 2023):154317. doi:10.1016/j.jcrc.2023.154317 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Dr. Michael Lanspa chats with Dr. Hannah Wunsch about her paper, "Evaluation of Etomidate Use and Association with Mortality Compared with Ketamine among Critically Ill Patients."

FAST24 | June 10 - 12, 2024 | Wilmington, North CarolinaFAST24 is our annual conference for pre-hospital and critical care transport professionals, including nurses, paramedics, and other disciplines. It features engaging workshops, talks by industry leaders, and focused sessions on air and surface critical care transport medicine. The event also offers a unique vendor experience, special guest appearances from notable talent in the industry, catered lunches, as well as relaxing and entertaining networking and social opportunities. Tickets are limited so don't wait! Visit https://fastsymposium.com for more information.The debate about which drug to use for sedation prior to RSI will.. just.. not… die. Advocates for both ketamine and etomidate approach the argument with near-religious zeal. There have been studies. We've even covered some here. What we need is a systematic review and meta-analysis, preferably using a type of analysis that recognizes that this likely isn't a black and white question and can bring some.. .nuance to it. That's were our friend Bayes comes in. Dr. Jarvis is joined by Drs Remle Crowe and CJ Winkler to discuss this paper and what in the hell Bayesian analysis actually is. We get some nice book recommendations in the process. Plus, we check in with ChatGPT for answers.Oh, BTW... don't take zoological advice from Dr. Winkler. Contrary to his thoughts, Giraffe's do NOT, in fact, have larger hearts than elephants. Citations:1. Koroki T, Kotani Y, Yaguchi T, Shibata T, Fujii M, Fresilli S, Tonai M, Karumai T, Lee TC, Landoni G, Hayashi Y. Ketamine versus etomidate as an induction agent for tracheal intubation in critically ill adults: a Bayesian meta-analysis. Crit Care. 2024 Feb 17;28(1):48. doi: 10.1186/s13054-024-04831-4. PMID: 38368326; PMCID: PMC10874027.2. Russotto V, Myatra SN, Laffey JG, et al. Intubation Practices and Adverse Peri-intubation Events in Critically Ill Patients From 29 Countries. JAMA. 2021;325(12):1164-1172.Bonus book recommendations3. Heller J. Catch-22. New York, NY: Simon & Schuster; 1961.4. McGrayne SB. The Theory That Would Not Die. How Bayes' Rule Cracked The Enigma Code, Hunted Down Russian Submarines & Emerged Triumphant From Two Centuries of Controversy. Yale University Press; 2011.5. Salsburg D. The Lady Tasting Tea: How Statistics Revolutionized Science In The Twentieth Century. Henry Holt & Company; 2001.

Show notes at pharmacyjoe.com/episode906. In this episode, I’ll discuss the mortality rate for critically ill patients when ketamine vs etomidate is used as an induction agent for intubation. The post 906: Does Using Ketamine for Induction Have a Lower Mortality Rate Than Etomidate? appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode906. In this episode, I’ll discuss the mortality rate for critically ill patients when ketamine vs etomidate is used as an induction agent for intubation. The post 906: Does Using Ketamine for Induction Have a Lower Mortality Rate Than Etomidate? appeared first on Pharmacy Joe.

Contributor: Travis Barlock MD Educational Pearls: Common sedatives used in the Emergency Department and a few pearls for each. Propofol Type: Non-barbiturate sedative hypnotic agonizing GABA receptors. Benefit: Quick on and quick off (duration of action is approximately 2-7 minutes), helpful for suspected neurologic injury so the patient can wake up and be re-evaluated. Also has the benefit of reducing intracranial pressure (ICP). Downsides: Hypotension, bradycardia, respiratory depression. What should you do if a patient is getting hypotensive on propofol? Do not stop the propofol. Start pressors. May have to reduce the propofol dose if delay in pressors. Dexmedetomidine (Precedex) Type: Alpha 2 agonist - causes central sedation Uses: Patients are more alert and responsive and therefore can be on BiPAP instead of being intubated. Does not cause respiratory depression. Downsides: Hypotension and Bradycardia. Caution in using this for head injuries, its side effects can mask the Cushing reflex and make it more difficult to spot acute elevations in ICP and uncal herniation. Ketamine Type: NMDA antagonist and dissociative anesthetic, among other mechanisms. Benefits: Quick Onset (but slower than propofol). Does not cause hypotension, but can even increase HR and BP (Thought to potentially cause hypotension if patient is catecholamine-depleted (ie. sepsis, delayed trauma)). Dosing ketamine can be challenging. Typically low doses (0.1-0.3mg/kg (max ~30mg)) can give good pain relief. Higher doses (for intubation/procedural sedation) are generally thought to have a higher risk of dissociation. Downsides: Emergence reactions which include hallucinations, vivid dreams, and agitation. Increased secretions. Benzos Type: GABA agonists. Benefits: Seizure, alcohol withdrawal, agitation due to toxic overdoses.  Push doses are useful because doses can stack. Longer half-life than propofol.   Downsides: Respiratory depression. Longer half-life can make neuro assessments difficult to complete. Etomidate MOA: Displaces endogenous GABA inhibitors. Useful as a one-time dose for quick procedures (cardioversion, intubation). Often drug of choice for intubation since it is thought to have no hemodynamic effects.  Downsides; If used without paralytic - myoclonus. Though to have some adrenal suppression. Fentanyl Type: Opioid analgesic. Not traditional sedative. Benefits: There are many instances in emergency medicine in which sedation can be avoided by prioritizing proper analgesia. Fentanyl can even be used to maintain intubated patients without needing to keep them constantly sedated. Downsides: Respiratory depression. Patients may have tolerance. References Chawla N, Boateng A, Deshpande R. Procedural sedation in the ICU and emergency department. Curr Opin Anaesthesiol. 2017 Aug;30(4):507-512. doi: 10.1097/ACO.0000000000000487. PMID: 28562388. Keating GM. Dexmedetomidine: A Review of Its Use for Sedation in the Intensive Care Setting. Drugs. 2015 Jul;75(10):1119-30. doi: 10.1007/s40265-015-0419-5. PMID: 26063213. Lundström S, Twycross R, Mihalyo M, Wilcock A. Propofol. J Pain Symptom Manage. 2010 Sep;40(3):466-70. doi: 10.1016/j.jpainsymman.2010.07.001. PMID: 20816571. Matchett G, Gasanova I, Riccio CA, Nasir D, Sunna MC, Bravenec BJ, Azizad O, Farrell B, Minhajuddin A, Stewart JW, Liang LW, Moon TS, Fox PE, Ebeling CG, Smith MN, Trousdale D, Ogunnaike BO; EvK Clinical Trial Collaborators. Etomidate versus ketamine for emergency endotracheal intubation: a randomized clinical trial. Intensive Care Med. 2022 Jan;48(1):78-91. doi: 10.1007/s00134-021-06577-x. Epub 2021 Dec 14. PMID: 34904190. Mihaljević S, Pavlović M, Reiner K, Ćaćić M. Therapeutic Mechanisms of Ketamine. Psychiatr Danub. 2020 Autumn-Winter;32(3-4):325-333. doi: 10.24869/psyd.2020.325. PMID: 33370729. Nakauchi C, Miyata M, Kamino S, Funato Y, Manabe M, Kojima A, Kawai Y, Uchida H, Fujino M, Boda H. Dexmedetomidine versus fentanyl for sedation in extremely preterm infants. Pediatr Int. 2023 Jan-Dec;65(1):e15581. doi: 10.1111/ped.15581. PMID: 37428855. Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMSII  

Background: Standard rapid sequence intubation (RSI) in the emergency department involves administration of an induction agent and a neuroblocking agent in quick succession.  RSI inherently carries with it risks of complications such as post-intubation hypotension and cardiac arrest in the most extreme cases.  It is possible that the induction agent used could play an important ... Read more The post REBEL Cast Ep120: Etomidate vs Ketamine for RSI in the ED? appeared first on REBEL EM - Emergency Medicine Blog.

Date: June3, 2023 Reference: Kotani et al. Etomidate as an induction agent for endotracheal intubation in critically ill patients: A meta-analysis of randomized trials. Journal of Critical Care April 2023 Guest Skeptic: Dr. Amber Gombash is an emergency physician in Concord, NC. Case: You have a critically ill patient that you are preparing to intubate and wonder […] The post SGEM#405: We're Off To Never-Never Land – But Should We Use Etomidate for the Rapid Sequence Intubation? first appeared on The Skeptics Guide to Emergency Medicine.

Show notes at pharmacyjoe.com/episode769. In this episode, I'll discuss alternatives to etomidate during the shortage. The post 769: Alternatives to etomidate during the shortage appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode769. In this episode, I ll discuss alternatives to etomidate during the shortage. The post 769: Alternatives to etomidate during the shortage appeared first on Pharmacy Joe.

Dr. Calvin Brown discusses recent research related to VL vs. DL, peri-intubation hemodynamic instability, and etomidate vs. ketamine in emergency endotracheal intubation.  He offers key take-away lessons, "Calvin's Critical Concepts", after each research topic is discussed.  

Introduction Pharmacology What does the Anesthesia Textbook Say? Evidence The post Episode 73. Etomidate for RSI in the Seizing Patient by Jimmy Pruitt appeared first on The Pharm So Hard Podcast.

Date: January 16th, 2022 Reference: Matchett, G. et al. Etomidate versus ketamine for emergency endotracheal intubation: a randomized clinical trial. Intensive Care Med 2021 Guest Skeptic: Missy Carter, former City of Bremerton Firefighter/Paramedic, currently a professor of Emergency Medical Services at Tacoma Community College's paramedic program. Missy is currently working in a community emergency department as a physician assistant and […]

It's the JournalFeed Podcast for the week of January 10-14, 2022. We cover the gender pay gap in EM leadership, subsegmental PE anticoagulation or not, a point/counterpoint on etomidate or ketamine firstline for RSI, and ketamine nebs for pain control.

Show notes at pharmacyjoe.com/episode672. In this episode, I’ll discuss ketamine vs etomidate for RSI. The post 672: Is there finally a clinically relevant reason to choose ketamine over etomidate for RSI? appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode672. In this episode, I’ll discuss ketamine vs etomidate for RSI. The post 672: Is there finally a clinically relevant reason to choose ketamine over etomidate for RSI? appeared first on Pharmacy Joe.

Ketamine IS AT LEAST as hemodynamically stable as ETOMIDATE!!!

Mit Etomidate kümmern wir uns um das nächste Medikament aus der Substanzklasse der Hypnotika. Das gewohnte Trio mit "möglicherweise Clemens", Dr. LADME Ralf und Ingmar kehrt die harten Fakten um Etomidate zusammen. Wäre da nicht diese Sache mit der Nebennierenrindeninsuffizienz wäre "Eto" sicher ein heißer Kandidat für einen Spitzenplatz in den Charts der Narkosemedikamente. Innerhalb von 4 Wochen nach Veröffentlichung können über die Website der Episode (https://ains.umg.eu/index.php?id=5166) Fortbildungspunkte beantragt werden.

What happens when/ if etomidate goes on shortage? Are methohexital or ketamine viable options for RSI in the ER? Find out this week.References:Farrell NM, Killius K, Kue R, et al. A comparison of etomidate, ketamine, and methohexital in emergency department rapid sequence intubation. J Emerg Med. 2020; 59(4): 508-514

Here is the JournalFeed Podcast for the week of August 3-7, 2020. We cover ketamine vs etomidate-related hypotension during induction, beta-blockers for refractory v-fib or v-tach, cerebral venous thrombosis score, and the end of the GI cocktail.

Etomidate

Etomidate

Show notes at pharmacyjoe.com/episode485. In this episode, I ll discuss whether etomidate can be given as a continuous infusion. The post 485: Can etomidate be given as a continuous infusion? appeared first on Pharmacy Joe.

This week Dr. Briggs and I talk about anesthesia, why you should learn stereochemistry, and how to win your Nobel Prize.

In this 132nd episode I welcome back Dr. Gillian Isaac to do more ABA keyword review. We review Spinals for the Basic Exam and Etomidate.

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 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 critically ill septic patients.  We should talk  briefly about the most common inciting infections that lead to sepsis. In order, these are: pneumonia, intra-abdominal infections, and urinary tract infections. No surprises there! Nachi: Yeah, that basically parallels my own experience, so that’s reassuring!  That takes us to our next potentially controversial topic - blood cultures.  Jeremy - we’re going to punt this one back to you Jeremy: This is another interesting topic that has received plenty of attention.   CMS loves blood cultures.  It’s an easy metric to track.  That doesn’t mean they’re always helpful.  We looked at our patients with lactates between 2.1 and 4.0 which had “severe sepsis.”  These patients were normotensive though, In other words, the ones that aren’t that sick.  We found that blood cultures are useful about 20% of the time.  That’s not bad.  So what do we do? We draw cultures before pushing antibiotics.  Is that helpful? Sometimes yes, does it waste money?  Debatable.  Does it help us meet our metrics, yes. Jeff: And I think that gets at the crux of the problem here: we don’t want to delay antibiotics on anybody, but we must balance this with the potential harm of further increasing the drug resistant bacterial population via sound antibiotic stewardship.  Remember also that there is a broad differential for sepsis, with several “sepsis mimics”. To name a few, we have PE, MI, CHF, acute pulmonary edema, DKA, thyroid storm, GI bleeds, drug intoxications, and withdrawal syndromes, just to name a few.  In case that wasn’t enough check out Table 3 of the article. Nachi:  And we already mentioned the leading causes of sepsis, that’s pneumonia, intra abdominal infections, and uti’s. But remember the source can be anywhere. Be sure to also think of pyelonephritis, central line associated bloodstream infections, prosthetics, endocarditis, necrotizing fasciitis, and meningitis. Jeff:  I don’t think we need to dwell on this much longer - basically the differential is huge.  Let’s move on to my favorite section - prehospital care. Jeremy: 20 pages of evidenced based recommendations and your favorite is the prehospital section, what’s up with that? Jeff: I’m an EMS fellow, what can I say… Anyway, on to my favorite section -- prehospital care.  This is always a hot topic because the prehospital period is a special opportunity to get early interventions in for septic patients  as 40 - 70% of all severe sepsis hospitalizations arrive via EMS. Nachi: And in one study taking place in a large metropolitan area, prehospital care time was over 45 minutes, and less than  37% arrived with IV access. Of course, these numbers would vary significantly based on where you practice. Jeff: So get this -- one study showed that out-of-hospital shock index and respiratory rate were highly predictive of ICU admission. So clearly early recognition and therapy may play a role here. Another study, however, showed knowledge gaps by advanced EMS providers in diagnosis and management of sepsis. And yet another study showed that only 18 to 21% of confirmed septic patients were suspected of having sepsis by EMS. Out of hospital fluids were started in only half of patients with severe sepsis. In essence, there is likely a strong role here for pre hospital protocols for identifying and treating sepsis. Nachi: In terms of pre hospital treatments though, prehospital IV fluids haven’t been shown to improve mortality, but have been associated with shorter hospital stays. Prehospital sepsis protocols have been described, but in general more research is needed in this area. Jeff: While prehospital care hasn’t yet been shown to improve the prognosis of septic patients, those presenting via EMS do have shorter delays to initiation of antibiotics, IV fluids, and early care bundles. EMS should focus primarily on stabilizing vital signs and providing efficient transport. If it’s possible to establish an IV and initiate fluids without delaying transport, EMS should do that as well. Nachi: And of course, oxygen for the hypoxic patients! Moving on to history and physical for your presumed septic patient. Jeremy, what are the big hitting things here that you always ask and check for, and that you make sure your residents are doing? Jeremy:  After ABC’s and glucose, AMS is really important, it’s in the QSOFA SCORE.  Unfortunately, this can be hard in many septic patients where they’re baseline mental status is less than perfect.  The other thing is to try and find the source.  Finding the source lets you make wise choices about therapy. Jeff:  Great point about the mental status - so many of our older population have an altered baseline, but recognizing changes from that baseline is key. Nachi:  Absolutely, with that in mind, let’s talk diagnostic studies, especially lactate.  Where I trained, basically everybody was getting a lactate, even tired looking residents seemed to be having their lactates checked, and trust me, they weren’t looking that good... Jeremy:  Brace yourself: lactate is really important in septic patients.  That being said, not every cause of elevated lactate is sepsis.  There is this animal called Type B lactic acidosis can come from numerous drugs like albuterol. Just because you see elevated lactate doesn’t mean you can forget about the other causes.  That being said, we know that patients with sepsis do better when they clear lactate. Jeff: Seems like the evidence is definitely in favor of serial lactate testing… Jeremy: For sure.  At least until you have a reasonable trend towards improvement.  We know lactate clearers do better.  We’ve looked at our own lactate numbers.  Interestingly, the takeoff point for sepsis seems to be around 2.5.  Meaning that patients with altered vitals and lactates above 2.5 tend to do worse.  But, there is a broad ddx to elevated lactate.   What is true, though, is that lactate is a marker for badness.  If your patient’s lactate is rising, yours should be too. Nachi: I bet I’m a “lactate clearer”. I may add “lactate clearer to my CV,” sounds impressive.  But I digress…  Next up we have Procalcitonin.   Since procalcitonin becomes elevated in those with bacterial infections, intuitively, this should be a valuable marker to assess in potentially septic patients.  Unfortunately procalcitonin lacks negative predictive value so most literature supports its use in diagnosing pulmonary infections and for antibiotic de-escalation. Jeff: Good to know, I’ve seen it being used a lot more recently and wondered how evidence based this test was. Jeremy:  Honestly, I don’t see Procalcitonin changing ED management at the moment.  If you’re   waiting for Procalcitonin to start antibiotics or fluids, you’re waiting too long. Nachi: Moving on, let’s talk imaging.  Based on current studies, the authors recommend focused imaging only.  In addition, they also note that our good friend, the point of care ultrasound, likely plays a role, as in one study, POCUS demonstrated a 25% improvement in sensitivity from clinical impression alone. Jeremy:  I think there are two ways POCUS comes in.  One, lung ultrasound can be really useful to find that occult pneumonia or differentiating pneumonia from CHF.   Two, your ultrasound is your best tool for assessing volume status.  I try to look at the IVC of all my septic patients and echo them when possible. Nachi: Right.  So now we’ve examined, drawn labs and cultures, checked a lactate, may be obtained imaging… next up we should probably start treating the patient. Whether you like it or not, we have to discuss CMS. Jeremy: Just to clarify before we start.  CMS defines “severe sepsis” as SIRS + infection with a lactate of 2.1-4.0. Septic shock is SIRS + infection with hypotension or a lactate > 4.0. That’s where we’re at. Jeff:  Good point.  Back to treatment: within the first 3 hours, for any patient with sepsis and septic shock, you must measure a lactate, obtain 2 sets of blood cultures, administer antibiotics, and give an isotonic fluid challenge with 30 cc/kg to patients with hypotension or a lactate greater than 4.   Then, within the first 6 hours, you must apply vasopressors to achieve a MAP of at least 65, re-assess volume status and perfusion, and remeasure a lactate. Nachi: This begs the question - are these recommendations evidenced based? Jeremy…. Jeremy: I’m so glad you asked that . Let’s start with fluids. Patient’s need adequate fluid resuscitation.  Interestingly there are 3 large RCT’s, PROMISE, PROCESS and ARISE,  that compared a Rivers type bundle to usual care.  Surprisingly, they showed no difference.  But when your drill down into these 3 trials, you see that “the usual care,” now generally includes at least 2 liters of fluid. Jeff: Ok, so it seems that there is some pretty good data to support a rapid fluid challenge of at least 30 cc/kg.  But how do we determine who needs more fluids and how much more they need.  There must be an endpoint to all of this? Jeremy: Another million dollar question. 30cc/kg is probably a good place to start.  How much is too much?  I think we need to be smart about our fluids.  Some patients will need less and some will need much more.  So, I remind my resident’s to be smart about fluids.  Sono an IVC, trend a lactate, follow a urine output, do a passive leg raise, even check JVP.  I mean just because you haven’t seen a unicorn doesns’t mean they’re not real.  Do something to monitor volume status. Nachi: Very important. Put your ultrasound skills to work here. They’ll only improve as you practice more.  Jeff, let’s get started on the ever important topic of antibiotics. Jeff: Sounds good.  Current guidelines recommend that broad spectrum antibiotics be administered within the first hour of presentation for those with sepsis or septic shock, ideally with blood cultures being drawn beforehand. In one study, every hour of delayed abx administration was associated with an 8% increase in mortality.  Since this 2006 study, other studies have had mixed results - with studies showing increased odds of death with delays in abx administration and others showing only a benefit in those with septic shock with or without hypotension with no benefit to those without shock. Nachi:  In terms of antibiotic coverage - you need to consider the site of infection, local resistance patterns, the presence of immunosuppression, and the patient’s age and comorbidities.  Table 5 of the article is very thorough and should be kept as a quick reference. Jeremy do you have any specific recommendations for our listeners on how we should approach antibiotic usage in the septic patient? Jeremy: I like to think about antibiotics a little more simply than referencing a table.  I ask a couple questions.  Does my patient need MRSA coverage ?  Does my patient need Pseudomonal coverage?  If the answer is no and no, then narrow your coverage.  You don’t necessarily have to use a bunch of Vanco, or a big gun antipseudomonal like Pip/tazo.  Also, have a look at your local antibiogram.  I can’t tell you how many times this changes prescribing habits for even things like simple UTIs.  I’m going to stray into some controversial territory here. The benefits of sepsis protocols are measured one patient at a time, but the harms are only measured in the aggregate.  What does that mean?  CMS metrics have caused us to  use to use more broad spectrum antibiotics.  As a result, we’re seeing more resistance.  My resident’s tell me to make it easy, give em VZ (that’s vanco/zosyn) and it kills me.   Every time you put a Z-pack into the world a pneumococcus gets it’s wings. So think more about your antibiotics, and know your local biograms. Jeff: That’s a great way to think about it, I fear I’ve given a lot of pneumococci wings during my training…  Next we’re on to vasopressors.  The data is pretty clear on this one - norepinephrine is the recommended first line vasopressor for septic shock.  In numerous trials comparing Norepi to dopamine, NE was far superior, with dopamine increasing arrhythmias in one trial and associated with an increased risk of death as compared to NE in another trial. Jeremy:  So here’s a question I get all the time: How can I give Norepi without a central line.  Let’s use Dopamine, its safe peripherally.  Ok, so follow that through.  We’re going to give a drug to increase blood pressure by constricting blood vessels, but don’t worry, it’s safe peripherally.  What does that mean?  It means it doesn’t work!!  It doesn’t give much blood pressaure.  Dopamine is a lousy pressor.  It causes a lot of tachycardia, which is not what you want in failing septic hearts.  So what do we do if we don’t have a central line?   We start norepi peripherally into a large bore IV for the time it takes us to get a central line.  That’s where the evidence is.  There’s a mortality benefit to NE over dopaine in septic shock. Jeff:  Right, this month’s authors note peripheral pressors may be safe for brief periods in settings with close monitoring.  While this is commonplace in some hospitals, others haven’t yet jumped on that bandwagon. I think it’s important to mention that this is becoming more and more commonplace, even in the prehospital realm.  With the service I fly for, we routinely start peripheral vasopressors without hesitation.  But this isn’t limited to the air.  Many ground 911 services have also adopted peripheral vasopressors in a variety of settings. Nachi: I’m sure there are many trials to come in the future documenting their safety profile, but moving on to the next pressor to discuss... vasopressin. This should be your second line vasopressor for septic shock.  In the VASST trial, low-dose vasopressin was found to be noninferior to NE.  In other trials, vasopressin also appeared to show a potential benefit in those with AKI and sepsis, although the subsequent VANISH trial (perhaps the best name for a clinical trial so far) failed to demonstrate a benefit to vasopressin titration with regard to renal outcomes in septic shock. Vasopressin has also been shown to reduce NE dosing when administered at a fixed dose of 0.03-0.04 units/min. Jeff: Next we have epinephrine.  In one study epinephrine and NE were equivalent in achieving MAP goals in ICU patients with shock, however several of those receiving epi developed marked tachycardia, lactic acidosis, or an increased insulin requirement.  The increasing lactic acidosis could confound the trending of lactates, so in those requiring inotropy in addition to some peripheral squeeze - the authors recommend adding dobutamine to norepinephrine instead of starting epinephrine. Although, keep in mind, this can lead to some hypotension so remember to start at low doses. Nachi: Phenylephrine, a pure alpha adrenergic agent, is next and should be considered neither first nor second line, but it may have a role as a push dose agent while preparing other vasoactive agents. Jeff: And lastly, we have angiotensin 2.  One recent 2017 study examining the role of angiotensin 2 in those with septic shock already on 0.2 mcg/kg/min of NE found that those receiving AT2 had significant improvements in MAPs as well as cardiovascular SOFA score at 48h with no difference in mortality.  Unfortunately, these benefits do not come without risk as AT2 may increase risk of arterial and venous thrombosis and potentially thromboembolism.  Clearly, one study isn’t enough to change practice, but it’s certainly food for thought. Nachi: So that wraps up vasopressors. Jeremy, we’re on to corticosteroids -- another hotly debated topic. When do you give steroids in sepsis? Jeremy:  Hmmm steroids, this is an age old question.  No study has clearly supported the blanket use of steroids in septic shock. Several like CORTICUS and ADRENAL showed no difference.  I will use hydrocortisone for pressor refractory shock. Meaning, you’ve tried everything else, so you might as well try.  Also, I do tend to avoid Etomidate, given the possibility of adrenal suppression and that there are several other induction agents, notably Ketamine  that don’t have this problem. Jeff: Those trials are certainly important, thanks for bringing them up - Especially with all the FOAM content out there, it’s incredibly important to look back at the data to understand where certain recommendations are coming from.   Anyway… one quick note on blood transfusions before we move on to special populations - Although part of the original early goal directed therapy, thanks to data from the TRISS trial which showed no difference in outcomes with a transfusion goal of 7 vs 9, transfusions are reserved for those with a hbg of less than 7. Jeremy:  One population we should make sure to mention and be careful with is end stage liver disease.  In the ER, we tend to miss SBP alot.  Mostly because these patients have lots of reasons to be sick and they already have elevated lactate because of their deceased clearance.  My practice is to give a dose of Ceftriaxone and sent a diagnostic tap to patients who are sick and have ascites. Nachi: Alright Jeremy, let’s talk controversies in sepsis. We’re giving you all the big questions this month! Jeremy:  We’ve already talked about fluids and how much to give.  Just a reminder that a history of CHF doesn’t preclude proper fluid resuscitation.  I think broad spectrum antibiotics for relatively well patients is a big controversy.  Our national rates of antibiotic resistance are terrible, and yet we’re using more antibiotics all the time.  There are very few if any antibiotics coming down the pharma pipeline and we’re going to have to face the music eventually.  Finally, we need national metrics that mirror clinical evidnece.  Protocols should be a tool and not a crutch.  You know what’s best for the patient in front of you, so don’t let metrics or protocols make you do things you think are not in your patient’s best interest. Nachi: So how do you escape the hospital protocols and CMS and do what’s best for your patient without “getting in trouble”? Jeremy: Here’s how I deal with it as the one who reads and QI’s all of our sepsis charts. I tell my colleagues to do what’s right, and if you need to deviate from the protocol tell me why.  As long as you can explain your decision, I’ll support it.  Explaining your thinking is good clinical practice and is good medico-legal practice. CMS has been unable to link these metric  to payment, simply because no hospital can meet them with any regularity.  It’s important that we advocate for our patients or nothing will change. Make them respect you for the highly educated professional that you are, and your patients will ultimately benefit. Jeff: Preach!! And before we close out with disposition, there are a few new therapies and trials on the horizon to keep a lookout for. The RACE trail examined the role of L-carinitine.  The VICTAS trial is looking at vitamin C, thiamine, and steroids in sepsis.  The CLOVERS trial is looking at early vasopressors vs a crystalloid liberal strategy.  And lastly, IL-7 is also being investigated.  All really cool stuff that could change how we manage sepsis in the future.. Nachi  A few quick notes on disposition before we close this episode out.  Certainly not all patients meeting SIRS require admission, but many do.  Those with qSOFA of 2 or higher represent a sick population and an ICU admission should be considered.   Even for those with a qSOFA of 1 but a lacate over 2 -- they have a mortality approaching that of patients with a qSOFA of 2.  Be careful just sending a patient who is on the fence to the floor because several studies have demonstrated that patients who are later upgraded have worse outcomes. Jeff: That’s in line with the general themes we’ve laid out today - definitely better to start early with aggressive care rather than play catch up later.  Jeremy - in 30 seconds or less, what are the most salient points in the management of sepsis that you would like our listeners to take with them from this episode. Jeremy:  Here are my take aways: qSOFA, RR, AMS SBP < 100 Norepi, not Dopamine - it doesn’t work! Be smart about fluids!! Be smarter about antibiotic use! You are the best advocate for your patient, despite what anyone else says! Jeff: Excellent, so that wraps up the October 2018 episode of Emplify. A big thanks to Jeremy Rose for joining us. Jeremy: Thank you for having me!!! It was great talking with you. Nachi: For our listeners -- additional materials are available on our website for Emergency Medicine Practice subscribers. If you’re not a subscriber, consider joining today. You can find out more at www.ebmedicine.net/subscribe. Subscribers get in-depth articles on hundreds of emergency medicine topics, concise summaries of the articles, calculators and risk scores, and CME credits. You’ll also get enhanced access to the podcast, including the images and tables mentioned. You can find everything you need to know at ebmedicine.net/subscribe. Jeff: And the address for this month’s credit is ebmedicine.net/E1018, so head over there to get your CME credit.  As always, the ding sound  you heard throughout the episode corresponds to the answers to the CME questions. Nachi: Lastly, be sure to find us on iTunes and rate us or leave comments there. You can also email us directly at emplify@ebmedicine.net with any comments or suggestions. Talk to you next month!

You're listening to the June edition of 3 Minute 3Rs, brought to you this month by Lab Animal (www.nature.com/laban), the NC3Rs (www.nc3rs.org.uk) and the North American 3Rs Collaborative (www.na3rsc.org). We're highlighting Drosophila as a microbiome model, organotypic brain culture slices for Alzheimer's research, and anesthesia for African clawed frogs. The papers behind the pod: * The Drosophila model for microbiome research: https://www.nature.com/articles/s41684-018-0065-0 * Preparation of organotypic brain slice cultures for the study of Alzheimer's disease: https://f1000research.com/articles/7-592/v1 * Comparison of Etomidate, Benzocaine, and MS222 Anesthesia with and without Subsequent Flunixin Meglumine Analgesia in African Clawed Frogs (Xenopus laevis): http://www.ingentaconnect.com/contentone/aalas/jaalas/2018/00000057/00000002/art00013 See acast.com/privacy for privacy and opt-out information.

In this episode I review the common IV agents used in anesthesia excluding opioids.  I cover Propofol, Barbiturates, Benzodiazepines, Ketamine, Etomidate and Dexmedetomidine. NOTE: There is an error in the audio recording regarding the dosing units for dexmedetomidine.  I say on the podcast that the dosing units are mcg/kg/min which is INCORRECT.  The correct dosing … Continue reading "Episode 10: IV Induction Agents"

Ep #21 Ketamine Induced Rapid Sequence Intubation with Faizan H. Arshad, MD @emscritcare Happy #EMSWeek #EMSStrong #EMSNation   SKEPTIC = Safety & Efficacy of Ketamine in Emergent Prehospital Tracheal Intubation – a Case Series   Brand new paper from Sydney HEMS on Ketamine and Shock Index in Annals of EM! http://www.annemergmed.com/article/S0196-0644(16)30002-6/abstract   Additional References: Carlson JN, Karns C, Mann NC, et al. Procedures performed by emergency medical services in the united states.Prehosp Emerg Care. 2015. Jacobs PE, Grabinsky A. Advances in prehospital airway management.International Journal of Critical Illness & Injury Science. 2014;4:57-64. Prekker ME, Kwok H, Shin J, Carlbom D, Grabinsky A, Rea TD. The process of prehospital airway management: Challenges and solutions during paramedic endotracheal intubation.Crit Care Med. 2014;42:1372-1378. Wang HE, Kupas DF, Greenwood MJ, et al. An algorithmic approach to prehospital airway management.Prehospital Emergency Care. 2005;9:145-155. Mace SE. Challenges and advances in intubation: Airway evaluation and controversies with intubation.Emerg Med Clin North Am. 2008;26:977-1000. Combes X, Jabre P, Jbeili C, et al. Prehospital standardization of medical airway management: Incidence and risk factors of difficult airway.Acad Emerg Med. 2006;13:828-834. Drummond GB. Comparison of sedation with midazolam and ketamine: effects on airway muscle activity. Br J Anaesth. 1996;76:663-667. Jackson APF, Dhadphale PR, callaghan ML, Alseri S. Haemodynamic studies during induction of anaesthesia for open-heart surgery using diazepam and ketamine. Br J Anaesth. 1978;50:375-378. Price B, Arthur AO, Brunko M, et al. Hemodynamic consequences of ketamine vs etomidate for endotracheal intubation in the air medical setting. Am J Emerg Med. 2013;31:1124-1132. Scherzer D, Leder M, Tobias JD. Pro-Con Debate: Etomidate or Ketamine for Rapid Sequence Intubation in Pediatric Patients. J Pediatr Pharmacol Ther. 2012;17:142-149. Bruder Eric A, Ball Ian M, Ridi S, Pickett W, Hohl C. Single induction dose of etomidate versus other induction agents for endotracheal intubation in critically ill patients.Cochrane Database of Systematic Reviews. 2015 Thompson Bastin ML, Baker SN, Weant KA. Effects of Etomidate on Adrenal Suppression: A Review of Intubated Septic Patients.Hospital Pharmacy. 2014;49:177-183. Arnold C. The promise and perils of ketamine research Ketamine began its life as an anaesthetic , but has enjoyed a recent renaissance as a potential. Lancet Neurol. 2013;12:940-941. Craven R. Ketamine. Anaesthesia. 2007;62:48-53. Perkins ZB, Gunning M, Crilly J, Lockey D, O’Brien B. The haemodynamic response to pre-hospital RSI in injured patients. Injury. 2013;44:618-623. Aroni F, Iacovidou N, Dontas I, Pourzitaki C, Xanthos T. Pharmacological Aspects and Potential New Clinical Applications of Ketamine: Reevaluation of an Old Drug. J Clin Pharmacol. 2009;49:957-964. Manthous CA. Avoiding circulatory complications during endotracheal intubation and initiation of positive pressure ventilation.J Emerg Med. 2010;38:622-631. Kohrs R, Durieux ME. Ketamine. Anesth Analg. 1998;87:1186-1193. Moy RJ, Clerc S Le. Trends in Anaesthesia and Critical Care Ketamine in prehospital analgesia and anaesthesia. Trends Anaesth Crit Care. 2011;1:243-245. Reich DL, Silvay G. Ketamine: an update on the first twenty-five years of clinical experience. Can J Anaesth. 1989;36(2):186-197. Porter K. Ketamine in prehospital care. Emerg Med J. 2004;21:351-354. Svenson JE, Abernathy MK. Ketamine for prehospital use: new look at an old drug. Am J Emerg Med. 2007;25:977-980. Johansson J, Sjöberg J, Nordgren M, Sandström E, Sjöberg F, Zetterström H. Prehospital analgesia using nasal administration of S-ketamine--a case series. Scand J Trauma Resusc Emerg Med. 2013;21:38. Filanovsky Y, Miller P, Kao J. Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury. Can J Emerg Med. 2010;12:154-201. Himmelseher S, Durieux ME. Revising a Dogma: Ketamine for Patients with Neurological Injury? Anesth Analg. 2005;101:524-534. Kropf J a., Grossman MD, Genzlinger M a., Stoltzfus J, Stehly CD. 328 Ketamine versus Etomidate for Rapid Sequence Intubation in Traumatically Injured Patients: An Exploratory Study. Ann Emerg Med. 2012;60:S117. Angus DC, van dP. Severe sepsis and septic shock.N Engl J Med. 2013;369:840-851. Jabre P, Avenel A, Combes X, et al. Morbidity related to emergency endotracheal intubation-A substudy of the KETAmine SEDation trial. Resuscitation. 2011;82:517-522. Shafi S, Gentilello L. Pre-Hospital Endotracheal Intubation and Positive Pressure Ventilation Is Associated with Hypotension and Decreased Survival in Hypovolemic Trauma Patients: An Analysis of the National Trauma Data Bank. The Journal of Trauma: Injury, Infection, and Critical Care. 2005;59:1140–1147. Seymour CW, Band RA, Cooke CR, et al. Out-of-hospital characteristics and care of patients with severe sepsis: A cohort study.J Crit Care. 2010;25:553-562. Williams E, Arthur a., Price B, Banister NJ, Goodloe JM, Thomas SH. 175 Ketamine versus Etomidate for Use in Helicopter Emergency Medical Services Endotracheal Intubation. Ann Emerg Med. 2012;60:S63-S64 Bruns, B, Gentilello, L, Elliott, A, Shafi, S. Prehospital Hypotension Redefined. The Journal of Trauma: Injury, Infection, and Critical Care. 2008;65:1217–1221. Seymour, CW, Cooke, CR, Heckbert, SR, et al. Prehospital Systolic Blood Pressure Thresholds: A Community-based Outcomes Study. Acad Emerg Med Academic Emergency Medicine. 2013;20:597–604. Kristensen AKB, Holler JG, Mikkelsen S, Hallas J, Lassen A. Systolic blood pressure and short-term mortality in the emergency department and prehospital setting: a hospital-based cohort study.Critical Care. 2015;1:158. Heffner AC, Swords DS, Neale MN, Jones AE. Incidence and factors associated with cardiac arrest complicating emergency airway management. Resuscitation. 2013;84:1500-1504. Salt PJ, Baranes PK, Beswick FJ. Inhibition of neuronal and extraneuronal uptake of noradrenaline by ketamine in the isolated perfused rat heart. Br J Anaesth. 1979;51:835-838. Sprung J, Schuetz SM, Stewart RW, Moravec CS. Effects of Ketamine on the Contractility of Failing and Nonfailing Human Heart Muscles in Vitro. Surv Anesthesiol. 1999;43:230-231. Kunst G, Martin E, Graf BM, Hagl S, Vahl CF. Actions of Ketamine and Its Isomers on Contractility and Calcium Transients in Human Myocardium. Anesthesiology. 1999;90:1363-1371. Lundy PM, Lockwood PA, Thompson G, Frew R. Differential Effects of Ketamine Isomers on Neuronal and Extraneuronal Catecholamine Uptake Mechanisms. Anesthesiology. 1986;64:359-363. Selde W. Push dose epinephrine. A temporizing measure for drugs that have the side-effect of hypotension.JEMS. 2014;39:62-63.   Sponsored by @PerfectCPR Apple Watch App with Audio and Haptic Feedback to Optimize Cardiac Arrest Training and Improve Quality of CPR Delivery PerfectCPR.com     Query us on Twitter: www.twitter.com/EMS_Nation Like us on Facebook: www.facebook.com/prehospitalnation   Wishing Everyone a safe tour! ~Faizan H. Arshad, MD @emscritcare www.emsnation.org  

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks: episteme, or theoretical knowledge, techne, or technical knowledge, and phronesis, or practical wisdom, also called prudence. Here we’ll invoke each type of knowledge and understanding as we go beyond the anatomical issues in pediatric airway management – to the advanced decision-making aspect of RSI and the what-to-do-when the rubber-hits-the road. Case 1: Sepsis Laura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother.  On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions.   Her heart rate is 160, RR 50, oxygen saturation is 88% on RA.  She has fine tissue-paper like rales throughout her lung fields.  Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse. She is in respiratory failure from bronchiolitis and likely viral sepsis.  She needs her airway taken over. Is this child stable enough for intubation? We have a few minutes to optimize, to resuscitate before we intubate. Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS.  Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child. Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV. Induction Agent in Sepsis The consensus recommendation for the induction agent of choice for sepsis in children is ketamine. Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock.  It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines. Paralytic Agent in Sepsis The succinylcholine versus rocuronium debate… Succinylcholine and its PROS 82% of RSI in the ED used succinylcholine (According to the National Emergency Airway Registry, in 2005).  We know it, we are comfortable with it. Succinylcholine produces superior intubating conditions when comparing 1 mg/kg succinylcholine versus 0.6 mg/kg rocuronium, succinylcholine is that at 45 seconds. Succinylcholine and its CONs Raises serum potassium in everyone, typically 0.5 to 1 mEq/L.  That is not usually a problem, but for those with preexisting or inducible hyperkalemia, it can precipitate an arrest, as in renal failure, underlying neurologic or myopathic conditions like multiple sclerosis, muscular dystrophy, ALS, or those who had a stroke or a burn more than 72 hours prior. We often have limited information in critical situations. Succinylcholine gives us a false sense of security.  In children, there really is no “safe apnea” period. Succinylcholine’s effect on the nicotinic receptors results in mydriasis, tachycardia, weakness, twitching and hypertension, and fasciculations (Think nicotine overdose: M/T/W/Th/F). Succinylcholine’s effect on muscarinic receptors manifest (as in organophosphate overdose): SLUDGE – salivation, lacrimation, urination, defecation, GI upset or more apropos here: DUMBBELLS – diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation. Second dose of succinylcholine – beware of the muscarinic effects and bradycardia. Co-administer atropine, 0.01 mg/kg, up to 0.5 mg IV. Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug.  The side effects are rare, but they can be deadly.  So, what’s the alternative? Rocuronium and its PROs It has none of the side-effects of succinylcholine Rocuronium and its CONs Argument 1: the duration is too long if there is a difficult airway, since rocuronium can last over an hour. Still need to intubate, and now your patient is potentially worse. Argument 2: succinylcholine produces better intubating conditions at 45 seconds compared to rocuronium. At 0.6 mg/kg, rocuronium is inferior to succinylcholine at all time intervals. At 1.0 mg/kg, rocuronium is still inferior at 45 seconds.  At 1.2 mg/kg rocuronium – the dose now commonly recommended – there was no difference in intubating conditions, per a study by Heier et al. in Anethesia and Analgesia in 2000. Case 2: Multitrauma Joseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him. He is brought in by paramedics, who are now bagging him. Induction Agent in Trauma Need something that is hemodynamically stable – agents such as midazolam or propofol would cause too many problems. Etomidate is a short-acting imidazole derivative that acts on GABA-A receptors to induce loss of consciousness in 5-15 seconds. It can cause apnea, pain on injection, and myoclonus. Etomidate reduces cerebral blood flow, reduces intracranial pressure, and reduces cerebral oxygen consumption, all while maintaining arterial blood pressure and cerebral perfusion pressure. Ketamine is reasonable as well: there is no contraindication to ketamine except for known hydrocephalus. It is safe in head trauma. It is a good choice for the hypotensive trauma patient.  TBI is not a contraindication. In the case of the critically injured child who is normotensive, ketamine will raise his blood pressure and perhaps foster further bleeding.  The goal is a good general perfusion and a balanced resuscitation, ensuring enough cerebral perfusion without disrupting nascent clots.  On the other side of the spectrum, permissive hypotension is not described in children, as hypotension is a late and dangerous sign of shock. Paralytic Agent in Trauma Are your surgeons in an uproar about a long-acting agent and the pupillary response?  Relax, it’s a myth. Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response.  Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response. In the critically ill, we rethink your dosing of both the sedative and the paralytic. In a critically ill child or adult, perfusion suffers and it affects how we administer medications.  The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives. We need to adjust our dosing for a critically ill patient: Decrease the sedative to avoid falling over the hemodynamic compensation cliff. Increase the paralytic to account for prolonged arm-brain time. Case 3: Cardiac/myocarditis/congenital heart disease Jacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing. The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology. The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump.  The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome. Typical “normal” saturations are 75 and 85% on RA.  Ask the parents or caregiver. Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others. A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism. Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive. Do we give fluids? Children after palliative surgery for cyanotic heart disease are volume-dependent.  Even if there is a component of cardiogenic shock, they need volume to drive their circuit.  Give a test dose of 10 mL/kg NS. Pressors in Pediatric Shock Children compensate their shock state early by increasing their SVR. Epinephrine (adrenaline) is great at increasing the cardiac output (with minimal increase in systemic vascular resistance; tachycardia)  In children the cardiac deleterious effects are not pronounced as in adults.  Later when the child is stabilized, other medication such as milrinone (ionotrope and venodilator) can be used. Epinephrine is also fantastic for cold shock when the patient is clamped down with cold extremities – the most common presentation in pediatric septic shock. Norepinephrine (noradrenaline) is best used when you need to augment systemic vascular resistance, such as in warm shock, where the patient has loss of peripheral vascular tone. Induction Agent in Cardiogenic Shock A blue baby – with a R –> L shunt – needs some pinking up with ketamine A pink baby – with a L –> R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate. Myocarditis or other acquired causes of cardiogenic shock – etomidate. Case 4: Status Epilepticus Jessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today. On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic. Induction Agent in Status Epilepticus Many choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol. Propofol as both a sedative and anti-epileptic agent works primarily on GABA-A and endocannabinoid receptors to provide a brief, but deep hypnotic sedation.  Side effects can include hypotension, which is often transient and resolves without treatment.  Apnea is the most common side-effect. Ketamine would be another good choice here, for its anti-epileptic activity. Paralytic Agent in Status Epilepticus Rocuronium (in general), as there are concerns of a neurologic comorbidity. Housekeeping in RSI What size catheter doe I use?  If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5. Remember this: 2, 3, 4 – Tube, Tape, Tap The NG/OG/Foley is 2 x the ETT – tube The ETT should be taped at a depth of 3 x the ETT size – tape A chest tube size 4 x the ETT – tap In summary, in these cases of sepsis, multitrauma, cardiogenic shock, and status epilepticus: Resuscitate before you intubate Use the agent’s specific properties and talents to your benefit Adjust the dose in critically ill patients: decrease the sedative, increase the paralytic Have post-intubation care ready: sedation, verification, NG/OG/foley

Anesthetic Induction with Etomidate, Rather than Propofol, Is Associated with Increased 30-Day Mortality and Cardiovascular Morbidity After Noncardiac Surgery

This episode is part 2 of the procedural sedation podcast. This episode focuses on the medications that we commonly use for procedural sedation. First, we'll review the use of oxygen during procedural sedation and then talk about basic airway maneuvers before we talk about individual medications. For each drug, the drug class, dosing, duration of action, and adverse effects will be discussed with the overall theme of patient safety.

For the second part of trauma resuscitation, we'll discuss the various interventions that you may have to accomplish in the trauma bay. The first part is a continuation from the first episode and talks about the EFAST exam- a vital part of the secondary survey. The second part discusses the control of massive extremity hemorrhage and how to intervene on any airway, breathing, or circulation issue in the trauma bay.

“Airway is the reason that many go into emergency medicine…”- Jaime McCarthy MD, UT Health Sciences Center at Houston EM DirectorOne of the many things that we do better than anyone in the business is obtain the emergent airway. Unlike our colleagues in other disciplines, we do not have the luxury of planning our airway approach on the golf course the evening before; we meet patients on their worst day. Even though we would often prefer it, we do not have the option to reschedule our intubations. Smashed, bloody, distorted, edematous, airways secondary to trauma, anaphylaxis and GI bleeds are the things that we deal with routinely with nary a complaint or even a hither for a better look than what were given. We often feel lucky to get any type of view that resembles normal laryngeal anatomy. Personally, if I knew that I would need to be intubated today, that my airway would be bloody and edematous, and there was only time for one person to take a shot at placing the tube, then I would pray to God that the last face I see before the Roc and Etomidate push me asunder is the familiar grill of one of my EM colleagues. Who better to bet all my chips on then someone who deals with the hardest airways on the face of the planet as part of their daily routine? The general EM provider can not only get that airway, but is so relaxed about it that they will casually check on the patient in the next bed before and after the intubation. That’s the confidence I’m looking for when it comes to the fast paced life and death world of emergency airway.Whether it is pediatric or adult emergency medicine, the most important thing that we do as “emergentologists and resusitologists” is control the airway. iTunes Link Mac Friendly Airway AlgorithmPodcast 6 - Pediatric Airway 101

81 Es wurden in dieser Studie bei 210 gynäkologischen tageschirurgischen Patientinnen intraoperative Wachheit und postoperative Erholung nach Kurznarkosen mit Etomdidate (n=50), Ketamin (n=10), Methohexital (n=50), Midazolam (n=49) und Propofol (n=51) untersucht. Um mögliche intraoperative Wachepisoden der Patientinnen erfassen zu können, wurden die Patientinnen entgegen dem klinischen Alltag während der Narkose aufgefordert, die Augen zu öffnen oder die Hand des Untersuchers zu drücken. Es wurde notiert, ob die Patientinnen daraufhin mit unspezifischen Aufwachreaktionen reagierten oder die Aufforderungen adäquat befolgten. Auch spontan aufgetretene Aufwachreaktionen wurden festgehalten. In dieser Studie wurden in allen fünf Hypnotikagruppen die gleichen Untersuchungstechniken angewendet. Die Pharmakodynamik und Pharmakokinetik der jeweiligen Hypnotika differierten allerdings teilweise erheblich und sind nicht immer ausreichend berücksichtigt worden, so dass die nachfolgend aufgeführten Ergebnisse kritisch zu bewerten sind und auf den klinischen Alltag zu übertragen sind. Bei dem hier angewandten Narkoseverfahren, d.h. Nachinjektionen der Anästhetika bolusweise anstatt als Dauerinfusion und nicht EEG-kontrolliert, fand sich, dass intraoperative Wachheit relativ häufig und unabhängig von der Art des Eingriffs bei Kurznarkosen mit Etomidate, Ketamin, Methohexital, Midazolam und Propofol auftrat: Von 210 untersuchten Patientinnen reagierten insgesamt 72% (152 von 210 Patientinnen) unspezifisch mit Aufwachreaktionen, spontan oder nach Ansprechen, oder befolgten gezielt Aufforderungen. Das Ausmaß der intraoperativen Wachheit hing bis zu einem gewissen Grad auch von dem verwendeten Hypnotikum ab: Die Zahl der intraoperativen Aufwachreaktionen und befolgten Aufforderungen lag in den untersuchten Patientinnengruppen zwischen 13,5% (Propofol) und 86% (Ketamin). Das Risiko, dass bei einer Patientin intraoperative Wachheit auftrat, erwies sich aufgrund der fehlenden EEG-Kontrolle als schwer einschätzbar: Bei einigen Patientinnen fehlten Anzeichen einer intraoperativen Wachepisode wie z.B. Unruhe oder spontane Aufwachreaktionen. Diese Patientinnen wirkten bewusstlos, befolgten aber auf Ansprache Aufforderungen. In allen Untersuchungsgruppen hätte das Auftreten intraoperativer Wachepisoden verringert werden können, wenn die Anästhetika per infusionem konstant verabreicht und sogar vermieden werden können, wenn die Narkosetiefe mittels EEG kontrolliert worden wäre. In dieser Studie wurden unterschiedliche Stufen intraoperativer Wachheit eingeteilt: a) Intraoperative Wachheit mit bewusster Erinnerung des Patienten daran 1. Erinnerbare bewusste Wachheit mit Schmerz

We determined the adrenostatic potential of low-dose nonhypnotic etomidate in six patients with Cushing's syndrome (ectopic Cushing's syndrome,n=2; Cushing's disease,n=3; bilateral adrenal adenoma,n=1). Etomidate was given as a continuous infusion for 32 h in a dose of 2.5 mg/h (n=5) or 0.3 mg/kg/h (n=3), respectively. Saline was given during a control period. The responsiveness to exogenous ACTH was studied during placebo and 7 and 31 h after commencing etomidate by administration of 250 µg 1–24 ACTH i.v. Etomidate (2.5 mg/h) led to a consistent decrease in serum cortisol in all patients from a mean of 39.4±13.3 to 21.1±5.7 µg/dl after 7 h (P