Podcasts about early management

Contributor: Travis Barlock MD Educational Pearls: Thrombolytic therapy (tPA or TNK) is often used in the ED for strokes Use of anticoagulants with INR > 1.7 or  PT >15 Warfarin will reliably increase the INR Current use of Direct thrombin inhibitor or Factor Xa inhibitor  aPTT/PT/INR are insufficient to assess the degree of anticoagulant effect of Factor Xa inhibitors like apixaban (Eliquis) and rivaroxaban (Xarelto)  Intracranial or intraspinal surgery in the last 3 months Intracranial neoplasms or arteriovenous malformations also increase the risk of bleeding Current intracranial or subarachnoid hemorrhage History of intracranial hemorrhage from thrombolytic therapy also contraindicates tPA/TNK Recent (within 21 days) or active gastrointestinal bleed Hypertension BP >185 systolic or >110 diastolic Administer labetalol before thrombolytics to lower blood pressure Timing of symptoms Onset > 4.5 hours contraindicates tPA Platelet count < 100,000 BGL < 50 Potential alternative explanation for stroke-like symptoms obviating need for thrombolytics References 1. Fugate JE, Rabinstein AA. Absolute and Relative Contraindications to IV rt-PA for Acute Ischemic Stroke. The Neurohospitalist. 2015;5(3):110-121. doi:10.1177/1941874415578532 2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients with Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke a Guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Vol 50.; 2019. doi:10.1161/STR.0000000000000211 Summarized by Jorge Chalit, OMSII | Edited by Jorge Chalit

In this episode, we review the role and indications of thrombolytics in acute ischemic stroke. The efficacy, safety, administration considerations, and cost between alteplase and tenecteplase are compared and contrasted. Key Concepts Alteplase (Activase) is a recombinant DNA version of human TPA (tissue plasminogen activator). Tenecteplase (TNKase) is similar to human TPA except it has three amino acid changes that result in a longer half-life and higher fibrin specificity. In patients with stroke, alteplase is given as a bolus followed by a 60-minute infusion. Tenecteplase is given as an IV bolus without the need for an infusion due to its longer half-life. Tenecteplase is at least as safe and effective as alteplase in acute ischemic stroke (with some studies showing greater benefit with tenecteplase). In patients with acute ischemic stroke who are candidates for mechanical thrombectomy, thrombolytics (with alteplase or tenecteplase) will still be given in patients who meet inclusion criteria and have no exclusion criteria. References Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association [published correction appears in Stroke. 2019 Dec;50(12):e440-e441]. Stroke. 2019;50(12):e344-e418. doi:10.1161/STR.0000000000000211 Campbell BCV, Mitchell PJ, Churilov L, et al. Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke. N Engl J Med. 2018;378(17):1573-1582. doi:10.1056/NEJMoa1716405 Kobeissi H, Ghozy S, Turfe B, et al. Tenecteplase vs. alteplase for treatment of acute ischemic stroke: A systematic review and meta-analysis of randomized trials. Front Neurol. 2023;14:1102463. Published 2023 Jan 23. doi:10.3389/fneur.2023.1102463

Caleb, Vann, and Luke sit down again with Dr. Rob Willson to discuss a serious problem in our adolescent athletes - patellar instability.  What happens when the kneecap moves out of its natural groove in the thigh bone (femur), either by contact or non-contact?  This is a serious injury in the young athlete and proper early management is the key to preserving the all-important articular cartilage that lives on the underside of the kneecap.  Dr. Rob Willson is an orthopedic surgeon with Augusta University.  He is fellowship-trained in Sports Medicine and is the team physician for the Augusta Greenjackets and all Augusta University athletics.Caleb Mellinger, PT,DPT,OCS, Luke Heusel, PT,DPT,OCS, and Vann Jordan, PT,DPT, OCS, all work at Peak Rehabilitation Fitness and Performance in Augusta, GA.www.Peakrehabfitperform.com

Contributor: Travis Barlock MD Educational Pearls:  Large Vessel Occlusion (LVO) is a condition where a clot blocks one of the major blood vessels in the brain, leading to a stroke. What are the vessels that can experience an LVO? Middle Cerebral artery (MCA) Internal Carotid Artery (ICA) Anterior Cerebral Artery (ACA) Posterior Cerebral Arteries (PCA) Basilar Artery (BA) Vertebral Arteries (VA) What are the locations at which a mechanical thrombectomy can be performed as a treatment for an LVO? Distal ICA, M1 or M2 segments of the MCA, A1 or A2 segments of the ACA, and some evidence for the BA. What are the symptoms of LVO? Use the mnemonic FANG-D to remember a few key symptoms: Field Cut (A person loses vision in a portion of their visual field) Aphasia (Difficulty speaking) Neglect (A person may have difficulty paying attention to or acknowledging stimuli on the affected side of their body or in their environment. For example, a person with neglect may deny that their left hand belongs to them) Gaze Deviation (One or both eyes are turned away from the direction of gaze) Dense Hemiparesis (Paralysis affecting one side of the body) What are the treatment windows for treating an LVO? 24 hours for mechanical thrombectomy 0-4.5 hours for tPA/TNK References 1. Brain embolism, Caplan LR, Manning W (Eds), Informa Healthcare, New York 2006. 2. Berkhemer OA, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015 Jan 1;372(1):11-20. doi: 10.1056/NEJMoa1411587. Epub 2014 Dec 17. Erratum in: N Engl J Med. 2015 Jan 22;372(4):394. PMID: 25517348. 3. Herpich, Franziska MD1,2; Rincon, Fred MD, MSc, MB.Ethics, FACP, FCCP, FCCM1,2. Management of Acute Ischemic Stroke. Critical Care Medicine 48(11):p 1654-1663, November 2020. 4. Warner JJ, Harrington RA, Sacco RL, Elkind MSV. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke. Stroke. 2019 Dec;50(12):3331-3332. doi: 10.1161/STROKEAHA.119.027708. Epub 2019 Oct 30. PMID: 31662117. 5. Hoglund J, Strong D, Rhoten J, Chang B, Karamchandani R, Dunn C, Yang H, Asimos AW. Test characteristics of a 5-element cortical screen for identifying anterior circulation large vessel occlusion ischemic strokes. J Am Coll Emerg Physicians Open. 2020 Jul 24;1(5):908-917. doi: 10.1002/emp2.12188. PMID: 33145539; PMCID: PMC7593424. Summarized by Jeffrey Olson | Edited by Meg Joyce & Jorge Chalit, OMS1  

Sepsis in other words ‘life-threatening organ dysfunction' in response to infection is a leading cause of death worldwide and a global health priority recognised by the World Health Organisation. In Australia, for adults with sepsis admitted to the intensive care unit, the in-hospital mortality is estimated as 18–27%. Early recognition of sepsis, prompt administration of antibiotics and resuscitation with intravenous fluids for those with features of hypoperfusion or shock are the mainstays of initial treatment. Emergency departments often being the first point of contact for patients presenting with sepsis, are required to prioritise sepsis as a medical emergency. The “Sepsis Kills” program implemented across the nation aims to reduce unwarranted clinical practice variation in management of sepsis.   In a recent Australian based study conducted across four emergency departments in Western Sydney Local Health District, among 7533 patients with suspected infection, a reduction in risk of in-hospital mortality was observed for each 1000 mL increase in intravenous fluids administered in patients with septic shock or admitted to ICU. However, despite evidence showing mortality benefits, not all aspects of sepsis care have been given the needed attention. In the same setting, out of 4146 patients with sepsis, 45% of them did not receive intravenous fluids in the emergency departments within the first 24 hours. Younger patients with greater severity of illness and presented to smaller hospitals were more likely to receive fluids.    The unanswered questions regarding the facilitators and barriers influencing intravenous fluid administration in sepsis are being explored using qualitative methods. Several emergency physicians and nurses have provided insight into aspects that influence their ability to provide appropriate fluid resuscitation such as constantly overcrowded emergency departments with chronic staff shortages of skilled health professional, failure to recognise sepsis early, the complexity of the presentations and lack of resources. Awareness of these challenges among stakeholders is the need of the hour. Leaving no one behind and not disregarding the critical aspects of sepsis care are crucial. Recognition of these factors and sustainable interventions are necessary to improve clinical outcomes for patients.   For more head to our podcast page #CodaPodcast

Managing winners and managing early at 21DTE both are great mechanics to improve performance. So what are the differences between these two approaches? Join Nick and Mike as they analyze the performances of using managing winners and managing early.

Managing winners and managing early at 21DTE both are great mechanics to improve performance. So what are the differences between these two approaches? Join Nick and Mike as they analyze the performances of using managing winners and managing early.

Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Michael Donovan, PhD, MD Diabetic kidney disease (DKD) can be burdensome for patients—especially if it progresses. How can we find out if our patients are at risk of progression? To answer that question, Dr. Charles Turck is joined by Dr. Michael Donovan to discuss a prognostic tool for type 2 diabetes patients with early-stage (stage 1-3b) chronic kidney disease.

Today let's talk a little about some considerations for the patient presenting with an acute ischemic stroke.  I've got a couple of references for you below as well!Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Updatehttps://www.ahajournals.org/doi/10.1161/STR.0000000000000211The Code Stroke Handbook: Approach to the Acute Stroke Patienthttps://www.amazon.com/Code-Stroke-Handbook-Approach-Patient/dp/0128205229/ref=sr_1_6?crid=3C5STQ82E9UYW&keywords=acute+stroke+hand&qid=1668425511&sprefix=acute+stroke+hand%2Caps%2C92&sr=8-6&ufe=app_do%3Aamzn1.fos.18ed3cb5-28d5-4975-8bc7-93deae8f9840 Find me on Twitter @Drkentris (https://twitter.com/DrKentris) Email me at theneurotransmitterspodcast@gmail.com https://linktr.ee/DrKentris The views expressed do not necessarily represent those of any associated organizations. The information in this podcast is for educational and informational purposes only and does not represent specific medical/health advice. Please consult with an appropriate health care professional for any medical/health advice.

Guest: Adam Oostema, MD MS FACEP (Associate Professor of EM, Michigan State University College of Human Medicine) Host: Jason Woods MD Select References: National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995 Dec 14;333(24):1581-7. doi: 10.1056/NEJM199512143332401. PMID: 7477192. Saver JL, Gornbein J, Starkman S. Graphic reanalysis of the two NINDS-tPA trials confirms substantial treatment benefit. Stroke. 2010 Oct;41(10):2381-90. doi: 10.1161/STROKEAHA.110.583807. Epub 2010 Sep 9. PMID: 20829518; PMCID: PMC2949055. Kwiatkowski TG et al. Effects of tissue plasminogen activator for acute ischemic stroke at one year. National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study Group. N Engl J Med. 1999 Jun 10;340(23):1781-7. doi: 10.1056/NEJM199906103402302. PMID: 10362821. Ingall TJ et al. Findings from the reanalysis of the NINDS tissue plasminogen activator for acute ischemic stroke treatment trial. Stroke. 2004 Oct;35(10):2418-24. doi: 10.1161/01.STR.0000140891.70547.56. Epub 2004 Sep 2. PMID: 15345796. Emberson J et al. Stroke Thrombolysis Trialists' Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29;384(9958):1929-35. doi: 10.1016/S0140-6736(14)60584-5. Epub 2014 Aug 5. PMID: 25106063; PMCID: PMC4441266. Hacke W et al. ECASS Investigators. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008 Sep 25;359(13):1317-29. doi: 10.1056/NEJMoa0804656. PMID: 18815396. Alper BS et al. Thrombolysis with alteplase 3-4.5 hours after acute ischaemic stroke: trial reanalysis adjusted for baseline imbalances. BMJ Evid Based Med. 2020 Oct;25(5):168-171. doi: 10.1136/bmjebm-2020-111386. Epub 2020 May 19. PMID: 32430395; PMCID: PMC7548536. Powers WJ et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec;50(12):e344-e418. doi: 10.1161/STR.0000000000000211. Epub 2019 Oct 30. Erratum in: Stroke. 2019 Dec;50(12):e440-e441. PMID: 31662037.

The probability of touch (POT) is the probability that at some point before expiration, the underlying price will reach the strike of the option. POT is calculated by multiplying the delta by two, so if you have a 10 delta put, the POT = 10 * 2 = 20%.Previously, we looked at the impact that early management had on probability of touch (POT), finding that when managing 16∆ options at 21 DTE, the POT was roughly equal to ½ the delta. But that was a small sample, simply looking at 16∆ calls and puts. What if we expanded the study?When managing early, can we estimate POT to be equal to ½ of delta? Or is there a different calculation that can apply broadly to all deltas?

The probability of touch (POT) is the probability that at some point before expiration, the underlying price will reach the strike of the option. POT is calculated by multiplying the delta by two, so if you have a 10 delta put, the POT = 10 * 2 = 20%.Previously, we looked at the impact that early management had on probability of touch (POT), finding that when managing 16∆ options at 21 DTE, the POT was roughly equal to ½ the delta. But that was a small sample, simply looking at 16∆ calls and puts. What if we expanded the study?When managing early, can we estimate POT to be equal to ½ of delta? Or is there a different calculation that can apply broadly to all deltas?

Podcast: Updates in Acute Stroke Management   Evaluation and Credit:  https://www.surveymonkey.com/r/MedChat36   Target Audience             This activity is targeted toward all physician providers.   Statement of Need Stroke is the fifth leading cause of death in the U.S. and Kentucky. Additionally, stroke is a leading cause of disability in the US. Kentucky residents exceed the national average for lifestyle habits that lead to stroke (smoking, obesity, etc.). Providers can benefit from understanding the latest treatment options in the acute management of strokes with the goal of maximizing patient outcomes.   Objectives At the conclusion of this offering, the participant will be able to: Define the types and causes of strokes. Describe the latest clinical protocols in the acute management of ischemic strokes.   Moderator Monalisa Tailor, M.D. Internal Medicine Norton Community Medical Associates   Speaker Danny Rose, M.D. Neurologist Norton Neurology Institute   Moderator and Planner Disclosures  The moderator, speakers and planners for this activity have no relevant relationships to disclose.   Commercial Support  There was no commercial support for this activity.   Physician Credits American Medical Association   Accreditation Norton Healthcare is accredited by the Kentucky Medical Association to provide continuing medical education for physicians.   Designation Norton Healthcare designates this enduring material for a maximum of 0.50 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.   Resources for Additional Study  Acute Stroke Intervention: A Systematic Review https://pubmed.ncbi.nlm.nih.gov/25871671/   Acute Stroke Management: Overview and Recent Updates https://pubmed.ncbi.nlm.nih.gov/34221544/   Scoping Review of Clinical Practice Guidelines for the Early Management of Stroke with Focus on Endovascular Treatment https://pubmed.ncbi.nlm.nih.gov/34418610/     Norton Healthcare, a not for profit health care system, is a leader in serving adult and pediatric patients throughout Greater Louisville, Southern Indiana, the commonwealth of Kentucky and beyond. Five Louisville hospitals provide inpatient and outpatient general care as well as specialty care including heart, neuroscience, cancer, orthopedic, women's and pediatric services. A strong research program provides access to clinical trials in a multitude of areas. More information about Norton Healthcare is available at NortonHealthcare.com.     Date of Original Release |February 2022 Course Termination Date | February 2024 Contact Information | Center for Continuing Medical, Provider and Nursing Education; (502) 446-5955 or cme@nortonhealthcare.org  

In this episode we get an update on how our Badminton athlete (from last week's episode) with achilles pain is doing after the initial evaluation. During the initial consult the athlete was educated on active recovery. What is Active Recovery? weekly newsletter for more rehab content Apply Now --> Application to Neuropedics' 12 Week Motor Control Mentorship Program Visit our website www.NeuropedicsPT.com Questions for Mez? You can email him: Ramez@NeuropedicsPT.com

In this episode we get into an interesting case study that Mez was asked to consult: A young female badminton athlete trying to qualify for the Olympics. We get into the nuances of how Mez sets up an evaluation to set the stage for establishing a therapeutic alliance via a thorough history before setting expectations and providing essential self care education. Blog Referenced in the episode: Active Recovery: What Is it? HERE for free sports rehab & fitness content. If you're sports PT and you're interested in our 12 week mentorship program email us at NeuropedicsPT@gmail.com Check out our website at www.NeuropedicsPT.com If you have any questions related to the episode content email Mez at Ramez@NeuropedicsPT.com

Our decision to manage trades at 21 days to expiration is derived from extensive research that holds with theoretical expectations and actual historical performance of OTM options. Because 75% of the profit of a SPY 16∆ strangle was realized by the trade's halfway point, on average, re-deploying capital in new positions has shown to generate more profits over time (since you'd be receiving 75% of potential P/L in 50% of the trade time).

Our decision to manage trades at 21 days to expiration is derived from extensive research that holds with theoretical expectations and actual historical performance of OTM options. Because 75% of the profit of a SPY 16∆ strangle was realized by the trade's halfway point, on average, re-deploying capital in new positions has shown to generate more profits over time (since you'd be receiving 75% of potential P/L in 50% of the trade time).

Margo Thienemann, MD is a Co-founder and Director of Psychiatric Services at for the Immune Behavioral Health/Pediatric Acute-Onset Neuropsychiatric Syndrome (IBH/PANS) Clinic at Stanford Children's Health and a Clinical Professor in Psychiatry and Behavioral Sciences Child and Adolescent Psychiatry in the Stanford School of Medicine. The clinic is the first PANS clinic in the country. Dr. Thienemann is an author and contributor to many PANS publications including the PANS Consensus Treatment Guidelines and PANS, Clinical Management of Pediatric Acute-Onset Neuropsychiatric Syndrome: Part I-Psychiatric and Behavioral Interventions. She has also written: Seeing Your First Child with PANDAS/PANS along with The PANDAS Physicians Network Diagnostics and Therapeutics Committee and with Stanford Continuing Medical Education, a free online CME activity: Presentation and Early Management of PANS. https://www.stanfordchildrens.org/en/doctor/margo-l-thienemann Join us Thursday nights at 8 PM EST on Instagram live @jowma_org for our latest podcast discussions!!

Margo Thienemann, MD is a Co-founder and Director of Psychiatric Services at for the Immune Behavioral Health/Pediatric Acute-Onset Neuropsychiatric Syndrome (IBH/PANS) Clinic at Stanford Children's Health and a Clinical Professor in Psychiatry and Behavioral Sciences Child and Adolescent Psychiatry in the Stanford School of Medicine. The clinic is the first PANS clinic in the country. Dr. Thienemann is an author and contributor to many PANS publications including the PANS Consensus Treatment Guidelines and PANS, Clinical Management of Pediatric Acute-Onset Neuropsychiatric Syndrome: Part I-Psychiatric and Behavioral Interventions. She has also written: Seeing Your First Child withPANDAS/PANS along with The PANDAS Physicians Network Diagnostics and Therapeutics Committee and with Stanford Continuing Medical Education, a free online CME activity: Presentation and Early Management of PANS. https://www.stanfordchildrens.org/en/doctor/margo-l-thienemann Join us Thursday nights at 8 PM EST on Instagram live @jowma_org for our latest podcast discussions!! This podcast is powered by JewishPodcasts.org. Start your own podcast today and share your content with the world. Click jewishpodcasts.fm/signup to get started.

Jason Scott and Stephen Vasquez, Sun-Maid Growers Technical Viticulturist, discuss the importance of managing powdery mildew early to avoid outbreaks like the ones growers saw in 2019. Powdery mildew is one of the most important fungal diseases impacting grape production in California, infecting green tissues such as leaves, shoots, rachises and berries.

"Screening and Early Management of Metastatic NSCLC: Updatesto Optimize Multidisciplinary Care"

"Screening and Early Management of Metastatic NSCLC: Updatesto Optimize Multidisciplinary Care"

Acute ischemic stroke is a leading cause of morbidity and mortality worldwide. Intensive care management of strokes is focused on reducing complications related to reperfusion treatment and decreasing secondary neurological injury. In this episode of Critical Matters, we will discuss the critical care management of acute ischemic strokes. Our guest is Dr. Sayona John, Associate Professor in the Department of Neurological Sciences at Rush Medical College. She is a practicing neurointensivist and also serves as the Head of the Section of Critical Care Neurology and Medical Director of the Neuroscience Intensive Care Unit & Neuroemergency Transfer programs at Rush University Medical Center in Chicago. Additional Resources: AHA 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: http://bit.ly/30TJkxL Educational video on performing the NIH Stroke Scale: http://bit.ly/2opldcZ Link to a pdf document with the NIH Stroke Scale: http://bit.ly/2LVtWMV How to do a four-minute neurological examination: http://bit.ly/328IXRr Books Mentioned in this Episode: Lincoln's Hundred Days: The Emancipation Proclamation and the War for the Union by Louis P. Masur: https://amzn.to/2VlTTse

Contributor: Dylan Luyten, MD Educational Pearls: Those that are hypokalemic are often hypomagnesemic, and should receive magnesium (Mg) supplementation if repleting potassium Mg levels are typically not necessary - if someone is suspect to have hypomagnesemia, just given them Mg Mg increases the AV node refractory period and therefore may be helpful as an adjunct to those in atrial fibrillation with a rapid ventricular response Mg is the preferred treatment for seizure prophylaxis in preeclampsia. All patients with suspected preeclampsia should get 4g Mg IV over 20 min Mg may reduce hospital admissions in those with severe asthma, though it has not shown to have mortality or other benefits in acute exacerbations Editor’s note: and we didn’t even touch on magnesium in headaches References Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007 Oct;18(10):2649-52. doi: 10.1681/ASN.2007070792. Epub 2007 Sep 5. Review. PubMed PMID: 17804670. Ismail Y, Ismail AA, Ismail AA. The underestimated problem of using serum magnesium measurements to exclude magnesium deficiency in adults; a health warning is needed for "normal" results. Clin Chem Lab Med. 2010 Mar;48(3):323-7. doi: 10.1515/CCLM.2010.077. PubMed PMID: 20170394. Heitz C, Morgenstern J, Bond C, Milne WK. Hot Off the Press: Low-dose Magnesium Sulfate Versus High Dose in the Early Management of Rapid Atrial Fibrillation: Randomized Controlled Double-blind Study. Acad Emerg Med. 2019 Sep;26(9):1093-1095. doi: 10.1111/acem.13720. Epub 2019 Mar 18. PubMed PMID: 30815951. Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations?. Ann Emerg Med.2015 Jun;65(6):702-3. doi: 10.1016/j.annemergmed.2014.07.019. Epub 2014 Aug 13. PubMed PMID: 25128007. Summarized by Will Dewispelaere, MS4 | Edited by Erik Verzemnieks, MD

Screening and Early Management of Metastatic NSCLC: Updates to Optimize Multidisciplinary Care

Screening and Early Management of Metastatic NSCLC: Updates to Optimize Multidisciplinary Care

Screening and Early Management of Metastatic NSCLC: Updates to Optimize Multidisciplinary Care

In episode 86 of Founder To Founder, Phil talks to former army special forces doctor turned entrepreneur Dr Dan Pronk.Dr Dan Pronk completed a Bachelor of Exercise Science at Griffith University in 1999 before studying medicine at Flinders University on an Army scholarship. Graduating with a Bachelor of Medicine and Bachelor of Surgery in Dec 2004, he continued at Flinders Medical Centre for his intern and first residency year. Dr Pronk entered into General Practice training in 2006, and subsequently completed his FRACGP in Jan 2011.In 2007 Dr Pronk posted to his first Army unit in Darwin as a Regimental Medical Officer. In 2008 Dr Pronk posted to 5 RAR in Darwin, and continued to serve with high-readiness infantry units in Sydney and Perth for the remainder of his full-time military career from 2009-2013. Dr Pronk deployed on operations on five occasions with the Army, once to Timor and the remainder to Afghanistan.During his military career Dr Pronk took a particular interest in the pre-hospital management of penetrating trauma, and had the privilege of representing the Australian Army at the NATO Special Operations Forces Medical Expert Panel.In 2014 Dr Pronk discharged from the full-time Army and commenced an MBA through University of South Australia, which he successfully completed in December 2016. In November 2014 Dr Pronk also successfully completed Early Management of Severe Trauma instructor training through the Royal Australian College of Surgeons, commencing instructing in September 2015.For the period of July 2014 - June 2015 Dr Pronk worked primarily in an Occupational Medicine role at BHPB's Olympic dam mine site in South Australia, whilst also working periodically offshore.In July 2015 Dr Pronk accepted a Senior Medical Officer role at a regional hospital in Queensland. He maintains his interest in tactical medicine through involvement with the Army School of Health's Care of the Battlefield Casualty program, as well as acting as a tactical medical consultant for various police and other government agency groups.In this episode Dan and Phil talk about how to manage being ‘in between’ ventures and transitioning from one life to another, how to manage the entrepreneurial rollercoaster and the three habits that founders need to develop to be successful.3 KEY POINTSDon’t underestimate the change an organisation needs to undertake from a team and culture perspective as it grows. This change needs to be managed and carefully and mindfully (12:03)There’s only one way to eat an elephant; one bite at a time. This is might sound cliche but it’s an effective way to thinking through events, challenges and opportunities that can be overwhelming (20:49)It’s not the critic that counts (26:35)By the way, if you'd like to know when new episodes are released or when Phil publishes his weekly long-form blog post, sign up for the insider's email list here: http://eepurl.com/drIF7r You can also follow Phil online:Website: https://philhsc.comInstagram: https://www.instagram.com/philhscLinkedIn: https://www.linkedin.com/in/philhscApple Podcasts: http://apple.co/2pc0GqJSpotify: http://spoti.fi/2AdJcPHGoogle Podcasts: http://bit.ly/2lGHaPKOvercast: http://bit.ly/2HhJAMXPocket Cast: https://pca.st/A7ZKMedium: https://medium.com/@philhsc

Well the year maybe coming to a close but the high quality papers keep on coming out! We've got 3 great articles to cover in this episode which have some key points to reflect on in our practice. First up we take a look at the application of Canadian c-spine rules by ED triage nurses and the potential impact this approach could hold. Next up we have a look at the addition of magnesium to current ED rate control of uncompromised patients presenting with rapid AF. Lastly we look at a paper on the conservative management of traumatic pneumothoraces, including those undergoing positive pressure ventilation, which reviews the complication rate of this approach. As always make sure you take a look at the papers yourselves and form your own opinions, we would love to hear you comments and feedback. Enjoy! Simon & Rob References & Further Reading Ian G. Stiell, Catherine M. Clement, Maureen Lowe, Connor Sheehan, Jacqueline Miller, Sherry Armstrong, Brenda Bailey, Kerry Posselwhite, Jannick Langlais, Karin Ruddy, Susan Thorne, Alison Armstrong, Catherine Dain, Jeffrey J. Perry, Christian Vaillancourt, 2018, 'A Multicenter Program to Implement the Canadian C-Spine Rule by Emergency Department Triage Nurses', Annals of Emergency Medicine, vol. 72, no. 4, pp. 333-341 Wahid Bouida, Kaouthar Beltaief, Mohamed Amine Msolli, Noussaiba Azaiez, Houda Ben Soltane, Adel Sekma, Imen Trabelsi, Hamdi Boubaker, Mohamed Habib Grissa, Mehdi Methemem, Riadh Boukef, Zohra Dridi, Asma Belguith, Semir Nouira, 2018, 'Low‐dose Magnesium Sulfate Versus High Dose in the Early Management of Rapid Atrial Fibrillation: Randomized Controlled Double‐blind Study (LOMAGHI Study)', Academic Emergency Medicine Steven P. Walker, Shaney L. Barratt, Julian Thompson, Nick A. Maskell, 2018, 'Conservative Management in Traumatic Pneumothoraces', Chest, vol. 153, no. 4, pp. 946-953 SGEM#232: I Can See Clearly Now the Collar is Gone – Thanks to the Triage Nurse London Trauma Conference; Cardiac Arrest Masterclass

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.

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!

La American Heart Association/American Stroke Association (AHA/ASA) publicó el 24 de enero del 2018 su más reciente actualización sobre el manejo del accidente cerebrovascular isquémico, titulada 2018 Guidelines for the Early Management of Patients with Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Estas guías están basadas en la mejor evidencia actualmente disponible, y aquí le proveemos un resumen de lo que usted debe saber. Para aquellos que seguimos el proceso de evaluación continua de la evidencia sobre atención cardiovascular de emergencia a través de eccguidelines.heart.org, sepa que las guías de manejo de accidente cerebrovascular no están en esa página. El documento de 344 páginas que discutimos en este artículo es una revisión completa de la literatura de stroke. Sin embargo, las guías de la AHA para el manejo de trombosis coronaria y cerebral son parte integral del contenido presentado en el curso de Soporte Vital Cardiovascular Avanzado (ACLS, por sus siglas en inglés). En este artículo revisaremos solamente los cambios nuevos relacionados al diagnóstico y terapia de reperfusión, pero el documento tiene todas las recomendaciones, incluyendo aquellas que no han cambiado desde la publicación de las recomendaciones del 2013 y la actualización enfocada del 2015. Es importante señalar que el documento antes mencionado es la verdadera referencia importante. La descripción aquí incluida no incluye las demás recomendaciones que no sufrieron cambios en esta edición. Para ver las recomendaciones completas, vea el documento original y completo. En el documento de la guía también aparecen descrito el significado de cada una de los niveles de recomendación y evaluación de la evidencia descritos luego de cada una de las recomendaciones (por ejemplo, "IIa C-EO"). En la carrera contra el tiempo, cada minuto perdido es cerebro perdido. El objetivo del manejo del accidente cerebrovascular es la reperfusión. Las dos alternativas de reperfusión primaria es la trombectomía y la fibrinolisis con alteplase (o tenecteplase). Telemedicina para consultar con expertos Es relativamente fácil tener alteplase en todos los hospitales. Pero es relativamente difícil poder tener neurólogos, neuroradiólogos y neurocirujanos disponibles en todas las facilidades. Pero en una era de telecomunicaciones y tecnología, esto no debe ser un problema. Debido a la distribución limitada y disponibilidad de expertos neurológicos, neuroquirúrgicos y neuroradiológicos, el uso de telemedicina/telestroke y sistemas puede ser beneficioso y debe ser apoyado por las instituciones de servicios de salud, gobiernos, pagadores y vendedores como un método de asegurar cobertura y cuidado adecuado 24/7 de pacientes con accidente cerebrovascular en una variedad de escenarios. IIa C-EO La guía hace una recomendación adicional sumamente importante: La administración de alteplase IV guiada por consulta de telestroke para pacientes con accidente cerebrovascular isquémico puede ser tan segura y beneficiosa como la de los centros de stroke. IIb B-NR Para los centros que no tienen telemedicina disponible, la guía del 2018 promueve la consulta por teléfono como una alternativa. Proveer apoyo en la toma de decisión sobre alteplase via consulta telefónica a médicos comunitarios es viable y segura, y puede ser considerarada cuando el hospital no tiene acceso a un equipo de accidente cerebrovascular presencial ni a un sistema de telestroke. IIb C-LD Esta declaración es importante porque promueve que las facilidades que no cuenten con los subespecialistas antes mencionados puedan comenzar con el tratamiento de alteplase previo a transferir el paciente al centro de stroke. Lo importante es comenzar la reperfusión dentro de la ventana de tiempo. Es más importante reperfundir primero que transferir primero. Tomografía (CT) en 20 minutos de la llegada El sistema debe ser establecido para que los estudios de imágenes cerebrales puedan ser realizados dentro de 20 minutos de la llegada al Departamento de Emergencias en al menos 50% de los pacientes que puedan ser candidatos a alteplase IV y/o trombectomía mecánica. I B-NR Según la guía, los estudios han demostrado que esto puede ser logrado en diferentes tipos de entornos hospitalarios. El signo de la arteria cerebral media (MCA) hiperdensa no debe ser usado para aguantar el alteplase IV a pacientes que, de otra manera, sí cualificarían. III B-R No se recomienda el uso de resonancia magnética para excluir microsangrados cerebrales antes de la administración de alteplase. III B-R Tomografía multimodal y resonancia magnética, incluyendo imágenes de perfusión, no deben retrasar la administración de alteplase IV. III B-R La tecnología es útil en la medida que sea efectiva y segura. La efectividad se mide aquí en la medida en que nos permite rápidamente tomar decisiones complejas. La seguridad consiste en el análisis riesgo vs beneficio. Imágenes para tratamiento endovascular Las Guías 2018 recomiendan el uso de angiografía por tomografía sin la valoración previa de la creatinina en pacientes sin historial previo de fallo renal. Nuevamente, la preferencia aquí es la velocidad en una población que tiene un riesgo muy bajo. Sin embargo, en pacientes entre 6 y 24 horas de la aparición de los síntomas, se pueden considerar otros estudios de resonancia magnética para valorar la selección de pacientes elegibles para trombectomía. Esto es parte de lo que demostró el estudio DAWN (Clinical Mismatch in the Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention With Trevo). Tenecteplase vs alteplase En la segunda parte de este artículo hablamos sobre la administración de alteplase. El alteplase se administra en una infusión que dura 1 hora. El tenecteplase, en cambio, se administra en bolo IV. En un estudio publicado en agosto del 2017 se demostró el tenecteplase no es superior al alteplase, y que tiene un perfil de seguridad similar al de alteplase en pacientes con un accidente cerebrovascular leve. El paciente con accidente cerebrovascular isquémico debe recibir alteplase IV, si es elegible, aún cuando se esté considerando la terapia endovascular y no se debe retrasar la terapia endovascular en espera de ver si hubo mejoría al administrar el alteplase. Trombectomía entre 6-24 horas El estudio DAWN mencionado anteriormente demostró que los pacientes que se levantan con signos de accidente cerebrovascular isquémico por oclusión de grandes vasos (LVO), y que no son elegibles para trombolíticos IV porque ya han pasado más de 4.5 horas, pueden ser elegibles a trombectomía. La trombectomía puede ser recomendada siempre y cuando haya evidencia de que hay cerebro viable y salvable. La recomendación en las primeras 16 horas es Clase I A. La recomendación hasta las 24 horas es IIa B-R. Terapia antiplaquetaria Si el accidente cerebrovascular es menor, y el paciente no va a recibir reperfusión primaria, la guía recomienda el uso de aspirina y clopidogrel (ambos) dentro de las primeras 24 horas del inicio del accidente cerebrovascular. También recomienda mantenerlo por 21 días como mecanismo de prevención de un segundo accidente cerebrovascular en los siguientes 90 días. Referencias http://stroke.ahajournals.org/content/early/2018/01/23/STR.0000000000000158 https://www.medscape.com/viewarticle/891786 https://professional.heart.org/idc/groups/ahamah-public/@wcm/@sop/@smd/documents/downloadable/ucm_498645.pdf

Two clinical scenarios in the “Education Practice” section of May's CGH look at approaches to acute pancreatitis during stages of early management and follow-up, respectively. Dr. Kuemmerle speaks with author Dr. Bechien U. Wu.

H. Bryant Nguyen, MD, associate professor of emergency medicine at Loma Linda University in California, discusses an article published in the April 2007 edition of Critical Care Medicine, Implementation of a Bundle of Quality Indicators for the Early Management of Severe Sepsis and Septic Shock is Associated with Decreased Mortality.(Crit Care Med. 2007;35(4):1105)