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Key Points Gamification in medical education can deeply engage learners and improve clinical skills. * Rapid Sequence alternates between game blocks, where learners act in clinical scenarios, and teaching blocks, where insights are shared. * True expertise is about developing effective cognitive strategies, not just accumulating knowledge. * Building mental models involves not just learning, but practicing decision-making in complex environments. * The learning environment should foster psychological safety and encourage growth through reflection and feedback. REBEL Rundown IntroductionWelcome back to Rebel MIND, the podcast where we sharpen the person behind the practitioner. MIND stands for Mastering Internal Negativity during D*ifficulty. This series emphasizes productivity, provider performance, and team optimization to ensure we are at our best during high-pressure situations.

In this episode, we introduce an innovative teaching tool called Rapid Sequence, aimed at revolutionizing how clinicians learn critical care through gamified experiences. With host Dr. Mark Ramzy, we invite Drs. Sarah Crager, and Ryan Ernst, to explore what it takes to become an expert and how gamification can transform learning in the medical field.

Cognitive QuestionWhat does it truly mean to be an expert in emergency and critical care medicine?

What Is Rapid Sequence?? It’s a gamified clinical case simulation tool consisting of different “blocks” where you have individual learners that can work through cases in non-multiple choice format. * You’re basically working on shifts, seeing multiple patients with your team. * There’s a cast of characters, interruptions, distractions, and you enter orders just like you would as if you were on shift, and then the cases advance to see the outcome of your decisions, good or bad * For more information check it out the Rapid Sequence website here. Use the following Promo Code: REBEL2026* at checkout page to receive a 20% off coupon

Figure 1: Screenshot from Rapid Sequence showing the initial dashboard

Learning Must Be An Active Not Passive Process* An important part of the process when acquiring new skills or information is making it an active process * It is not just passively listening, but actively participating, providing answers that aren’t multiple choice, and then responding to the outcome * This provides the engagement, and increases both the comprehension and retainability of new concepts * When you then apply those same concepts in future times of questioning (or in Rapid Sequence’s case “Blocks”) it helps expedite active recall through spaced repetition How This Applies to the Emergency Department or ICU?In high-stakes environments like the ED or ICU, clinicians must make fast, informed decisions often without complete data. Rapid Sequence provides a simulated space where clinicians can make mistakes without risk to real patients, receive feedback, and build the cognitive resilience needed for actual shifts, mirroring the chaotic nature of these departments.

Immediate Action Steps for Your Next Shift1. *Embrace Gamified Learning*: Engage with or seek out platforms like Rapid Sequence that offer a practice ground for real-world medical scenarios. 2. *Develop Mental Models*: Start by breaking down complex cases into mental models that you can refer back to during your shift. 3. *Prioritize Feedback and Reflection*: After each shift, allocate time to reflect on decisions and seek peer feedback to refine your cognitive strategies. 4. *Foster a Safe Learning Environment*: Encourage open discussions in your team where all members can express uncertainties and learn from one another. ConclusionEmbracing innovative teaching methodologies such as gamification can lead to significant improvements in clinical education and practice. By integrating tools like Rapid Sequence in training, healthcare professionals can not only enhance their skills but also foster a culture of continuous learning and psychological safety.

Clinical Bottom LineEffective medical education isn’t about rote memorization—it’s about developing the ability to think critically and adapt rapidly in ever-changing environments. Gamified tools offer an engaging path to achieve true expertise, ensuring clinicians are well-equipped to provide the best patient care possible.

Meet the Authors Sara Crager, MDAssociate Professor, Critical Care and Emergency MedicineUCLA, Los Angeles, CA * * * Ryan Ernst, MDAssistant Professor of Emergency Medicine, Section Chief of Global EMUniversity of Utah, Salt Lake City, UTShowing Slide 1 of 2The post REBEL MIND – Teaching Towards Expertise with Gamification appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points Mastery Learning: A unique educational framework focusing on achieving high competence with minimal variability among learners. * Deliberate Practice: Involves learner-driven improvement, guided by expert feedback and breaking skills down into micro steps. * Psychological Safety: Essential in mastery learning, allowing open feedback without fear or shame, enhancing growth. Embrace the productive struggle! * Practice to Prevent Skill Decay and Improve Clinically*: Application of mastery learning principles helps maintain high proficiency levels in both common and rare procedures. Click here for Direct Download of the Podcast.

Previously Covered and Related Content: REBEL MIND: The Dunning-Kruger Effect * REBEL MIND: Growth vs Fixed Mindset IntroductionWelcome back to Rebel MIND, the podcast where we sharpen the person behind the practitioner. MIND stands for Mastering Internal Negativity during Difficulty. This series emphasizes productivity, provider performance, and team optimization to ensure we are at our best during high-pressure situations. In this episode, host Dr. Kim Bambach chats with master educator Dr. Jennifer Yee about the science of performance through mastery learning and deliberate practice.*

Jennifer Yee, DO is an associate residency program director for OSU Emergency Medicine, the OSU EM director for assessment and evaluation, and an associate professor of emergency medicine. She is from Akron, Ohio and earned her bachelor degree from Ohio University and her medical degree through the Ohio University College of Medicine. Her residency training was completed through Summa Akron City Hospital. After serving as chief resident, she completed a simulation medicine fellowship at Summa.

She completed Northwestern’s Designing and Implementing Simulation-Based Mastery-Learning Curricula, as well as Ohio State’s Master of Art’s program in Biomedical Education. She established a mastery-based procedural curriculum for OSU’s EM residency program before creation of an institution-wide mastery-based central venous catheter (CVC) curriculum for all housestaff expected to place CVCs during their clinical training.

Cognitive QuestionHow can use the principles of mastery learning as better benchmark for learning, performance, and patient safety? How can we practice deliberately?

What is Mastery Learning?Unlike traditional clinical training, which is time-bound (e.g., “you are competent after a 3-year residency” or “after 10 chest tubes”), Mastery Learning is outcome-bound. The goal is to get every single learner from their unique baseline to an identical, objectively high level of performance with minimal variation. In this framework, learners start with a pre-brief, followed by baseline assessment, targeted debrief, deliberate practice, and a final evaluation using a checklist with a strict minimum passing standard (often set via methods like the Mastery Angoff). The mastery learning framework has been shown to improve patient safety.

• • The Northwestern Central Line Study: Research demonstrated that requiring residents to achieve a set benchmark on a simulator prior to clinical performance led to fewer needle passes, a decrease in mechanical complications (such as accidental arterial punctures), and a subsequent reduction in catheter-associated infection rates in the intensive care unit.

  • High-Acuity, Low-Occurrence (HALO) Procedures: Studies have demonstrated that for rare, critical procedures like emergency cricothyrotomies or transvenous pacing, baseline testing shows that very few trainees can meet a standard passing score initially. However, following targeted simulation training and deliberate practice, 100% of participants successfully achieved the minimum standard required to perform the procedure competently. The Anatomy of Deliberate Practice * + We often assume experience or confidence equals competence, but humans are notoriously poor self-assessors (plug for our Dunning-Kruger episode!). True deliberate practice isn’t just repeating a task for 10,000 hours; it is purposeful, learner-driven micro-skill improvement guided by an expert coach.

    • High-Quality Feedback: Avoid vague phrases like “good job” or “read more.” Effective coaching relies on strictly objective, real-time observations (e.g., “I am watching your needle angle. If you enter the skin more steeply, you will hit the vessel faster”).
    • Embrace a Growth Mindset: Stripping away your ego to be silently watched and critiqued is inherently awkward. Normalize deliberate practice to create psychological safety. Overcoming this requires building an environment centered on patient safety, where baselines are treated as data points rather than judgments. True growth happens with the “productive struggle”.
    • Adaptive Expertise: True mastery means moving past a rigid checklist. It requires learners to understand the reasoning behind their actions and anticipate next steps, complications, and plot twists in real time. Immediate Action Steps for Your Next Shift1. *Reflect on Personal Goals*: Identify specific clinical skills you wish to improve and set objectives.
    • *Seek Expert Feedback*: Find a mentor or coach for guided practice and objective feedback on your skills.
    • *Cultivate Psychological Safety*: Foster an environment where discussing mistakes and receiving feedback is viewed as growth rather than criticism.
    • *Practice Adaptively*: Introduce scenarios with atypical anatomy, complications, plot twists to better prepare for real-world complexity. ConclusionBy focusing on specific skill improvement and welcoming constructive feedback, clinicians can build competence and confidence, ultimately improving performance and patient safety. Effective mastery learning hinges on creating psychologically safe learning environments, engaging in focused deliberate practice, and leveraging expert feedback. This approach can be applied to clinical procedural excellence as well as many other skills, including communication and team dynamics.

Clinical Bottom LineMastery learning is an outcome-bound framework to reach a high standard of performance and deliberate practice is the tool that can help you achieve that high performance through expert feedback.

Further Reading1. Barsuk JH, et al.
Dissemination of a simulation-based mastery learning intervention reduces central line-associated bloodstream infections. BMJ Quality & Safety. Sep 2014.
PMID: 24632995 2. Klein MR, et al.
Developing simulation-based mastery learning curricula for emergency medicine skills training. AEM Education and Training. Jun 2025.
PMID: 40521339 Meet the Authors Kim Bambach, MDAssistant Professor of Emergency MedicineThe Ohio State University Wexner Medical Center, Columbus, OH Jennifer Yee, DOAssociate Professor of Emergency Medicine, Associate Program DirectorThe Ohio State University Wexner Medical Center, Columbus, OHShowing Slide 1 of 2The post REBEL MIND – Mastery Learning and Deliberate Practice appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL RundownClick here for Direct Download of the Podcast.

What Is Nitrous Oxide?Nitrous Oxide (N2O) is a colorless, odorless inhaled anesthetic that has been used for centuries, particularly in the surgical world. Mechanistically, it can induce euphoria, anxiolysis, and intoxication via NMDA receptor antagonism.

During the late twentieth century, nitrous oxide was increasingly used recreationally due its accessibility and perceived benign nature.

The modern day slang term for nitrous oxide is “whippets” – which tends to refer to the canisters that contain this agent and are frequently used as whipped cream foaming agents.

Despite the legal nature and benign perception of nitrous, frequent use can lead to lasting and permanent neurologic effects.

How Nitrous Oxide Causes ToxicityNitrous oxide toxicity results from its ability to oxidize the cobalt moiety in Vitamin-B12, thus leading to a functional B12 deficiency, despite adequate consumption and absorption.1

Functioning B12 is needed as a cofactor for methionine synthase.2 This enzyme has two critical roles:

The conversion of 5-methyl tetrahydrofolate to tetrahydrofolate; tetrahydrofolate is essential for the synthesis of our DNA.

And the conversion of homocysteine to methionine; methionine is needed to maintain the integrity of the myelin sheath of our axons.

As a result, nitrous toxicity leads to: a megaloblastic anemia and demyelination of both the dorsal columns and the lateral corticospinal tracts (also known as subacute combined degeneration).

Clinical Manifestations of Nitrous Oxide ToxicityThese patients will have a combination of both upper and lower motor neuron symptoms due to demyelination of the dorsal columns, lateral corticospinal tracts, and peripheral nerves. As a result, the following may manifest:

Dorsal Columns: diminished sense of proprioception, vibration, and fine touch.

Lateral Corticospinal Tracts: upgoing plantars, hyperreflexia, weakness of voluntary distal muscle control

Peripheral Nerves: numbness/tingling and weakness in a glove and stocking pattern (symptoms that start initially in the feet and hands that progressively spread proximally to the ankles and wrists)

Taking all of this into account, patients may present with difficulty ambulating, positive Romberg sign, dysmetria (difficulty with finger to nose or heel to shin), upgoing Babinski reflex, and decreased strength and sensation in a glove and stocking pattern.

How to Diagnose Nitrous Oxide NeurotoxicityHistory is key! As with a lot of pathologies in toxicology, identifying the exposure will expedite management.

A thorough neurologic exam will narrow the differential – with a particular focus to fine, peripheral motor and sensory deficits, dysmetria, proprioception, and ability to ambulate.

Magnetic resonance imaging of the spine may identify enhancement and/or edema of the dorsal columns, specifically on T2 weight axial imaging – sometimes referred to as the “inverted V” or “inverted rabbit ears appearance.”3

Serum B12 concentrations may be normal as the issue is with a functional deficiency as opposed to a vitamin absence. However, patients have elevated concentrations of both homocysteine and methylmalonic acid, both of which are metabolized in the presence of functional B12.

Management of Nitrous Oxide ToxicityFirst and foremost, cessation of nitrous oxide abuse is crucial to limit/prevent toxicity.

While there is no universally agreed upon treatment regimen, supplementation with intramuscular B12 is recommended.

Approaches vary from daily or every other day injections until symptoms improve at which point injections can be spaced out to weekly and then monthly.

Physical and occupational therapy may be needed depending on the degree of functional debility.

It is important to note, that depending of the severity and chronicity of toxicity, some proportion of patients may not fully return to their baseline.

Take-Home Points Though legal and seemingly benign, nitrous oxide abuse can lead to permanent neurologic dysfunction. * Nitrous oxide toxicity can affect the dorsal columns, lateral corticospinal tracts, and peripheral nerves. * Thus leading to a constellation of both upper and lower motor neuron deficits, particular in a glove and stocking pattern: deficits in proprioception and fine motor skills, positive Romberg, upgoing Babinski, peripheral numbness, tingling, and weakness. * Magnetic resonance imaging may identify symmetric high signal intensity in the dorsal columns. * Treatment includes B12 supplementation and physical/occupational therapy as needed. References1. Long H. Chapter 81. Inhalants. In: Nelson LS, et al. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019 2. Shah K, Murphy C. Nitrous Oxide Toxicity: Case Files of the Carolinas Medical Center Medical Toxicology Fellowship. J Med Toxicol. 2019 Oct;15(4):299-303. doi: 10.1007/s13181-019-00726-x. Epub 2019 Aug 6. PMID: 31388940; PMCID: PMC6825085. 3. Schmitz ZP, Hoffman RS. Magnetic resonance imaging in a patient with nitrous oxide-induced subacute combined degeneration of the spinal cord. Clin Toxicol (Phila). 2023 Nov;61(11):1006-1008. doi: 10.1080/15563650.2023.2286205. Epub 2023 Dec 19. PMID: 38060330. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)*

Associate Editor###### Anand Swaminathan

MD, MPHAll Things REBEL EM

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Procedures and SkillsRead MoreShowing Slide 1 of 7The post REBEL Core Cast—Nitrous Oxide Toxicity: Whippets and Neurologic Injury appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points Human Factors: The unseen behaviors, distractions and considerations critical in emergency medicine and the ICU, influencing patient care beyond just medical knowledge.

System Design: Effective system design directly impacts team performance by creating environments that facilitate optimal decision-making.

Real-world Application: The application of human factors in healthcare leads to better team dynamics, reduced stress, and improved patient outcomes.

It’s Everyone’s Job: Building a culture of adaptability and openness to change can lead to better healthcare delivery, communication and interprofessional relationships

Practical Solutions: Start the conversation in departments for actionable and pragmatic changes to current healthcare environments to enhance practitioner efficiency and patient care quality.

Click here for Direct Download of the Podcast.

Previously Covered and Related Content: + REBEL EM: Titles Don’t Make Leaders + REBEL MIND: Moving from Junior to Senior Leadership in Emergency Care + REBEL MIND: The Dunning-Kruger Effect + REBEL MIND: Growth vs Fixed Mindset IntroductionWelcome back to Rebel MIND, the podcast where we sharpen the person behind the practitioner. MIND stands for Mastering Internal Negativity during D*ifficulty. This series emphasizes productivity, provider performance, and team optimization to ensure we are at our best during high-pressure situations. In this episode, host Dr. Mark Ramzy chats with special guests and master educators about the concept of human factors.

Dr. Chris Hicks is an emergency physician and trauma team leader at St. Michael’s Hospital in Toronto, Assistant Professor in the Department of Medicine at the University of Toronto, and co-founder of Advanced Performance Healthcare Design, a physician-led simulation and design group. Dr. Andrew Petrosoniak is an emergency physician and trauma team leader at St. Michael’s Hospital, and Medical Director of the Unity Health Toronto Simulation Program. He’s an Assistant Professor at the University of Toronto where his research focuses on simulation for systems and design improvement and optimizing the care of the bleeding patient. Along with Dr. Hicks, he’s also President of Advanced Performance Healthcare Design, a consulting firm that works with high-performance teams and uses simulation to enhance and design better healthcare spaces

Cognitive QuestionHow can the integration of human factors improve decision-making and performance in emergency medicine and critical care environments?

What are Human Factors?In the context of healthcare, human factors encompass the interplay between humans, the systems they work within, and the effectiveness of their interactions. It includes elements like communication, system design, environmental conditions, and behavioral patterns affecting individual and team decision-making processes. It’s the collective impact of individual behaviors, team dynamics, and the physical environment on performance and outcomes. The aim is to eliminate issues arising from human error by creating systems and environments that naturally guide and support optimal performance.

How This Applies to the Emergency Department or ICU? + Efficient integration of human factors in high-pressure settings like the Emergency Department (ED) or Intensive Care Unit (ICU) helps mitigate the risks associated with stressful and chaotic environments. + By focusing on system designs that account for human behavior, healthcare professionals can reduce errors, enhance team coordination, and ultimately improve patient care. + This is crucial as teams are often required to make rapid, life-saving decisions in these environments + The design of clinical spaces can either hinder or help efficient care. Poorly arranged equipment or cluttered workspaces increase stress and impede decision-making. + Implementing structured design principles, such as dedicated equipment zones and clear visual cues, can streamline workflows and enhance team coordination + It actually helps pave the way for more efficiency because you end up “working smarter instead of harder”. - It speaks directly to the Daniel Kahneman’s theory of Type 2 Thinking – which is a slow, analytical cognitive process requiring deliberate thought - We’ll likely create a whole dedicated episode to this but if you want to read more ahead of time on it, check out his book Thinking, Fast and Slow Immediate Action Steps for Your Next Shift1. Assess Your Environment: Take note of any clutter, noise, or layout issues in your workspace that could hinder optimal performance. Identify problem areas that could be optimized. 2. Recognizable Hard-Stop – Implement a “Stop-Point” Check for areas or issues that involve more than just patient safety (ie. workflow inefficiencies, sign-out, throughput, etc). Use predefined benchmarks during procedures to ensure clarity and efficiency. 3. Foster Open Communication – Encourage an environment where every team member feels comfortable discussing their thoughts and decisions without fear of judgment. 4. Prototype Solutions – Work with colleagues to identify problems and brainstorm quick, cost-effective solutions that could be tested in your department. 5. Role Clarity and Preparation – Ensure roles are clearly defined and team members are prepared with necessary resources readily available during high-stakes scenarios. 6. Test and Refine* – Conduct quick pilot tests of new setups or processes during quieter times and gather feedback from your team. ConclusionHuman factors play a critical role in shaping healthcare outcomes. Through structured system designs and attention to team dynamics, it is possible to reduce inefficiencies and enhance both patient care and provider well-being.

It requires a shift in perspective from seeing design and systems as separate from human behaviors, to seeing them as intricately linked. By incorporating these principles, healthcare professionals can create environments that inherently support better, safer, and more effective patient care.

Clinical Bottom LineIncorporating human factors into healthcare isn’t just about preventing errors—it’s about creating an ecosystem where the healthcare team is empowered to perform at their best, even under the most challenging conditions. Implementing small, iterative changes can create a meaningful impact, paving the way for improved systems and processes.

This starts by redesigning systems and environments with human factors in mind, which can significantly improve both the efficiency of care delivery and the safety of the healthcare environment.

Further Reading1. Petrosoniak A, Hicks C.
M&M rounds 2.0: the future of performance improvement. CJEM. Feb 2025
*PMID: 39979684 2. Petrosoniak A, Hicks C
Design, build, train, excel: Using simulation to create elite trauma systems. International Anesthesiology Clinics. Publish Ahead of Print.
Request the Article here 3. Petrosoniak A, Hicks C, et al.
Design Thinking-Informed Simulation: An Innovative Framework to Test, Evaluate, and Modify New Clinical Infrastructure. Simul Healthc. 2020 Jun 2020.
PMID: 32039946 4. Bleetman A, et al.
Human factors and error prevention in emergency medicine. Emerg Med J. May 2012
PMID: 21565880 5. Hayden EM, et al.
Human Factors and Simulation in Emergency Medicine. Acad Emerg Med. 2018 Feb 2018
PMID: 28925571 Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ * * Chris Hicks, MD, MedCo-Founder of Advanced PerformanceAssistant Professor of Emergency Medicine, University of Toronto, Canada* Andrew Petrosoniak, MD, MScCo-Founder and President of Advanced PerformanceMedical Director of Unity Health Toronto Simulation ProgramShowing Slide 1 of 3The post REBEL MIND – Human Factors: The Hidden Architecture of Emergency & Critical Care Medicine appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points Parallel Tasking: Transitioning from junior to senior roles in medicine involves both personal growth and the development of leadership skills, often simultaneously.

Psychological safety: Creating this within teams is critical for fostering an environment where all members feel empowered to speak up and share insights.

Big and Small Picture View: Effective leadership requires the ability to zoom in on specific tasks and zoom out to manage the big picture, ensuring comprehensive patient care.

Timing is Everything: The act of asking the right questions at the right time can significantly enhance team dynamics and patient outcomes in high-pressure situations.

Talk the Talk: Creating and practicing clear, structured communication strategies can assist in smooth transitions and effective leadership during medical emergencies.

Click here for Direct Download of the Podcast.

Previously Covered and Related Content: REBEL EM: Titles Don’t Make Leaders * EM Cases: Four Key Learnings from a Career in Emergency Medicine Leadership IntroductionWelcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during D*ifficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. Hosted by Dr. Mark Ramzy, with special guest Dr. Dan Dworkis, an emergency physician and author of “The Emergency Mind,” this episode dives into the complex journey from junior to senior leadership in medical settings.

You can learn more about Dan’s work and the Emergency Mind Project here

He has a phenomenal book called “The Emergency Mind: Rewiring Your Brain for Performance Under Pressure“ that you can purchase here!

Cognitive QuestionHow do medical professionals effectively transition from junior to senior roles, and what mental shifts are necessary to manage these evolving responsibilities?

How This Applies to the Emergency Department or ICU? + Transitioning from a junior to a senior role in the emergency department or ICU is akin to stepping onto a new stage where the performance demands are higher, and the stakes significantly greater. + While juniors focus on learning their craft and understanding themselves, seniors are expected to manage and lead entire teams, often making life-saving decisions under pressure. + This transition challenges not only their clinical skills but also their ability to lead effectively and maintain psychological safety within their teams. + By fostering an environment where every team member feels valued and heard, senior leaders can harness the collective intelligence of the group, ensuring better patient outcomes and a more effective response to emergencies. Immediate Action Steps for Your Next Shift1. Exercise Intentional Questioning: Start your next shift by focusing on how you ask questions. Aim to frame queries in a way that invites discourse and challenges assumptions. 2. Develop Peripheral Awareness: As you conclude critical tasks, practice expanding your focus from the immediate to the wider context, considering broader departmental needs. 3. Promote Inclusive Participation: Encourage junior team members to share their observations and insights by specifically inviting their input during debriefs and planning. 4. Conduct Leadership Experiments: On your next shift, try altering your leadership approach—whether it’s how you communicate or delegate—and reflect on its effectiveness with colleagues. 5. Create Psychological Safety*: Work towards fostering a safe environment for open communication, ensuring that all team members feel comfortable speaking up without fear of retribution. ConclusionTransitioning from a junior to a senior leadership role in the medical field is not just about honing your clinical skills but also about growing as a leader who can guide a team under intense pressure.

By focusing on intentional communication, fostering psychological safety, and keeping an eye on both the details and the bigger picture, you can enhance your effectiveness as a leader.

Continuous reflection and feedback are essential to mastering these skills, ensuring that both you and your team provide the highest level of care for your patients.

Clinical Bottom LineLeadership in medicine is about more than making decisions—it’s about creating an atmosphere where every voice is heard, ensuring optimal functioning of the team.

As you grow into your senior role, remember that fostering psychological safety and practicing strategic communication can make all the difference in patient outcomes and team dynamics.

Further Reading1. Collins-Nakai R. Leadership in medicine. Mcgill J Med. 2006 Jan;9(1):68-73. PMID: 19529813 2. Chen TY. Medical leadership: An important and required competency for medical students. Tzu Chi Med J. 2018 Apr-Jun. PMID: 29875585 Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ* * * Dan Dworkis, MD, PhDFounder of Emergency Mind ProjectAssistant Professor at Keck School of Medicine at USC and Chief Medical Officer at Mission Critical Team Institute * Showing Slide 1 of 2The post REBEL MIND – The Mental Jump: Moving from Junior to Senior Leadership in Emergency Care appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL RundownKey Points Growth mindset transforms learning – Residents and students who believe skills can be developed are more open to feedback, more resilient after failure, and more engaged in practice. * Language matters in feedback – Simple reframes such as “You’re developing procedural skills” instead of “You’re not strong at procedures” encourage persistence and normalize the learning curve. * Mindset shapes team culture – Growth mindset leaders foster psychological safety, invite input, and create collaborative teams. Fixed mindset hierarchies, on the other hand, silence voices and can compromise patient care. * Growth mindset protects against burnout – By reframing mistakes as part of the process, clinicians reduce perfectionism and shame, bolstering resilience and wellness. * Practical steps start with self-talk – Add the word “yet” to limiting beliefs (“I’m not good at X…yet”) and shift feedback questions toward improvement (“What’s one thing I can do better next time?”). * Embracing mistakes with a growth mindset* – Leads to more effective feedback loops and improvement do this by building a culture of psychological safety is crucial for growth and reducing medical errors. Click here for Direct Download of the Podcast.

Previously Covered and Related Content: + REBEL EM: The EM Mindset + REBEL EM: Titles Dont Make Leaders + REBEL EM: Mind of the Resuscitationist with Scott Weingart + EM Crit: Making Things Happen with Cliff Reid IntroductionWelcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during D*ifficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine.

Mindset shapes everything we do in medicine—from how we teach and learn to how we show up for patients at the bedside. Drawing from Carol Dweck’s influential book Mindset, this episode of REBEL MIND explores the critical difference between a fixed mindset (believing abilities are innate and static) and a growth mindset (seeing skills as things that can be developed through effort and feedback).

We sat down with Dr. Kim Bambach, an emergency medicine physician and medical educator, and Dr. Frank Lodeserto, a dual-trained intensivist and internal medicine program director, to unpack how mindset influences medical education, bedside performance, and physician wellness. In this episode, we delve into how the mindset of clinicians can profoundly influence their performance, professional growth, and ultimately patient care

Cognitive QuestionHow does adopting a growth versus a fixed mindset influence clinical performance, medical education and patient outcomes?

What is Growth vs Fixed Mindset? + In Carol Dweck’s research, two primary mindsets are highlighted: - Fixed mindset: Which sees intelligence and skills as static * In the medical field, adopting a fixed mindset might lead a clinician to avoid complex cases due to fear of failure. * Growth mindset: Which views abilities as improvable through dedication and effort. + In contrast, a growth mindset encourages embracing challenges as opportunities for learning and development. How This Applies to the Emergency Department or ICU? + In high-stakes environments like the ICU or the ED, the mindset adopted by healthcare providers can distinctly shape patient care and team dynamics. + A fixed mindset might lead to defensive behaviors and a reluctance to engage in challenging cases, potentially stunting personal and professional growth. + Conversely, a growth mindset not only fosters resilience and adaptability but also enhances team collaboration and patient outcomes by encouraging open communication, continuous learning, and acceptance of constructive feedback. Immediate Action Steps for Your Next Shift1. *Monitor Self-Talk: Notice your internal narrative when faced with challenges. Replace negative, fixed-mindset thoughts with growth-oriented ones like “Not yet” or “What can I learn from this?” 2. Promote a Culture of Inquiry: Challenge yourself and your team to engage in constructive questioning and explore alternative diagnoses or treatment plans to encourage a growth-centered environment. 3. Model Vulnerability: Share personal learning experiences and mistakes with colleagues to normalize the growth process and reduce the stigma of imperfection. 4. Reframe Feedback: Instead of broadly asking, “How did I do?” inquire, “What’s one thing I can improve on next time?” This shift helps maintain focus on growth rather than performance validation * + - * + Feedback is a whole another topic that we plan to have dedicated episodes and blog posts. This is an area where sometimes faculty struggle and often learners are asking for more/improved feedback.* ConclusionCultivating a growth mindset in medicine isn’t merely about staying positive; it’s about embracing continuous learning in the face of challenges. It involves creating supportive environments that encourage vulnerability, experimentation, and resilience. By adopting these practices, clinicians can improve not just personal competencies but also enhance patient care quality and safety.

Clinical Bottom LineClinicians who embrace a growth mindset not only enhance their skills but also contribute to a more dynamic, adaptive, and error-resilient healthcare environment. Remember, the best clinicians are those who never stop learning, not the ones who never make mistakes.

Episode Audio Edited By: Kim Bambach, MD and Mark Ramzy, DO (Twitter/X/IG: @MRamzyDO) Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_Propersi)

Further Reading and References1. Claro S, Paunesku D, Dweck CS.
Growth mindset tempers the effects of poverty on academic achievement. Proc Natl Acad Sci U S A. 2016 Aug 2. Epub 2016 Jul 18.
PMID: 27432947 2. Blackwell LS, et al.
Implicit theories of intelligence predict achievement across an adolescent transition: a longitudinal study and an intervention. Child Dev. 2007 Feb; PMID: 17328703 3. Hopkins SR, et al. Trainee growth vs. fixed mindset in clinical learning environments: enhancing, hindering and goldilocks factors. BMC Med Educ. 2024 Oct 23
PMID: 39443909 4. Memari M, Gavinski K, Norman MK.
Beware False Growth Mindset: Building Growth Mindset in Medical Education Is Essential but Complicated. Acad Med. 2024 Mar 1. Epub 2023 Aug 30.
PMID: 37643577 Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ* * * Kimberly Bambach, MDAssistant Professor of Emergency MedicineThe Ohio State University Wexner Medical Center, Columbus, OH Frank Lodeserto, MDInternal Medicine Residency Program DirectorCape Fear Valley Medical Center, Fayetteville, NCShowing Slide 1 of 3The post REBEL MIND – Growth vs Fixed Mindset in Medicine appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points POCUS diastology answers one ED question: Is left atrial pressure (LAP) elevated right now? (not “diagnose diastolic dysfunction”) * E/e’ estimates LAP using mitral inflow E (PW Doppler) and annular e’ (TDI) from an apical 4-chamber view * Interpretation: E/e’ ≥ 14 → likely elevated LAP (supports cardiogenic pulmonary edema); ≤ 8 → LAP likely normal; 8–14 → indeterminate * Fast + actionable: With a decent apical view, E and e’ can be captured in ~60 seconds to guide diuresis/afterload reduction vs non-cardiac pathways * Use context: E/e’ performs best in reduced EF and can be confounded by MR/MS, tachycardia, and BiPAP/PEEP IntroductionA formal echocardiographic diagnosis of diastolic dysfunction is multivariable, nuanced, and not an ED priority* in most acute dyspnea cases.

In the emergency setting, the bedside question that changes management is simpler:

Is left atrial pressure (LAP) elevated right now?

Elevated LAP is the physiologic substrate for cardiogenic pulmonary edema and the target for therapies like diuresis and afterload reduction. “POCUS diastology” is a focused ultrasound approach that helps you answer that question quickly—often faster than CXR, BNP, or a “CHF vs pneumonia” radiology impression.

POCUS diastology ≠ chronic diagnosis.It’s a real-time estimate of filling pressure to guide acute resuscitation.

Case: Acute dyspnea with an unclear storyA 72-year-old obese woman presents with severe dyspnea. EMS placed her on BiPAP for hypoxia. She’s uncomfortable, with bibasilar crackles and faint wheezing.

Vitals: BP 166/98, HR 110, RR 22, SpO₂ 86%.

Your differential is broad:

• Pneumonia?
• COPD exacerbation?
• Flash pulmonary edema?

CXR: “Atypical pneumonia vs pulmonary edema” (not helpful)

Labs: WBC 14.1, pBNP 320 (still not helpful)

Your bedside ultrasound:

• The IVC is dilated → tempting to anchor on CHF

But you pause: COPD on BiPAP can also dilate the IVC via increased intrathoracic pressure and RV loading.

You obtain a cardiac view:

• EF looks normal → but that doesn’t rule out elevated filling pressures (hello HFpEF physiology)

Does this settle it? Can we give this patient bronchodilators, steroids and antibiotics?

The goal of POCUS diastologyYou’re not trying to label the patient with “diastolic dysfunction.”

You’re asking one resuscitation question:

Is LAP elevated in this moment?

If yes → cardiogenic pulmonary edema becomes much more likely and diuresis/afterload reduction moves up the priority list.

If no → search hard for non-cardiogenic causes (COPD, pneumonia, PE, ARDS, etc.).

Pathophysiology RefresherDiastolic filling depends on:

• Intrinsic: LV relaxation, LV compliance, atrial contraction
• Extrinsic: pericardial pressure, RV function, intrathoracic pressure (BiPAP), volume status

When the LV is stiff/noncompliant, blood backs up into the LA → LAP rises → pressure transmits to the pulmonary vasculature → pulmonary edema.

This can happen even with normal EF.

The POCUS method: E/e’ to estimate LAPTo estimate LAP, you measure:

• E wave: early diastolic mitral inflow velocity (PW Doppler)
• e’ wave: early diastolic mitral annular tissue velocity (TDI)

Then calculate:

E/e’ = Mitral inflow (E) ÷ Mitral annular velocity (e’)This ratio is used as a noninvasive estimate of LV filling pressures and correlates with formal echocardiography-derived estimates.

Example formula cited in echo literature:

LAP ≈ (1.24 × E/e’) + 1.9

Important nuance (keep your wording tight):

E/e’ can be used in both preserved and reduced EF, but performance is generally stronger in reduced EF. In normal EF, treat E/e’ as a high-value clue rather than a standalone verdict—especially in the intermediate zone.

Spectral Doppler feels intimidating (so let’s make it practical)A lot of POCUS users avoid Doppler because it feels “advanced.”

Here’s the reality:

If you can obtain a decent apical 4-chamber, you can obtain E and e’.

Once the view is good, capturing waveforms is straightforward.

Step-by-step: How to get E and e’ in under 60 secondsMitral inflow E wave (PW Doppler)1. Obtain an apical 4-chamber view Best view: interventricular septum appears vertical 2. Place the sample gate at the mitral leaflet tips If view isn’t perfectly parallel with flow of blood, consider using Doppler angle correction. 3. Activate Pulse Wave Doppler4. Freeze the tracing & Identify: E = early filling wave * A = atrial contraction wave 5. Measure peak E velocity Take the average of 3 measurements to be more precise. Mitral e’ wave (Tissue Doppler)1. From the same apical 4-chamber view, switch to TDI & place the gate at the septal mitral annulus2. Identify e’ (early diastolic annular motion) To accommodate the inflow of blood, the annulus moves basally and away from the probe. * The waveforms will always be negatively deflected 3. Measure peak e’ velocity Take the average of 3 measurements to be more precise. Interpreting E/e’ (cutoffs) Resus scenario: back to the bedsideYou obtain your images:

• E wave = 110 cm/s
• e’ = 5 cm/s
• E/e’ = 22

That strongly supports elevated LAP and therefore cardiogenic pulmonary edema physiology.

Action: You prioritize IV diuresis (and consider afterload reduction as appropriate), while avoiding reflexive bronchodilators/steroids/antibiotics as your default path.

Result: The patient’s breathing improves within 30 minutes—less diagnostic drift, fewer unnecessary meds, and potentially fewer intubations.

FAQ1. What is E/e’ on ultrasound?E/e’ is the ratio of mitral inflow (E wave) to mitral annular tissue velocity (e’). It’s used to estimate LV filling pressures and left atrial pressure. 2. What E/e’ value suggests elevated filling pressure?
An E/e’ ≥ 14 supports elevated LAP; ≤ 8 suggests normal LAP; 8–14 is indeterminate and should be integrated with other findings. 3. Can E/e’ be used with preserved EF (HFpEF)?
Yes, but it’s generally less reliable than in reduced EF. In HFpEF, treat E/e’ as a strong clue—especially when very high—while integrating the full clinical picture. 4. Why not just use BNP or CXR?BNP and CXR can be nonspecific or delayed. E/e’ targets physiology (filling pressure) at the bedside when it matters most. 5. Why aren’t we talking about the E/A ratio?The E/A ratio can be misleading because of the phenomenon of pseudonormalization. In grade 2 diastolic dysfunction the E/A ratio reverts from abnormal to normal; this can be a clinical trap. Bottom Line POCUS diastology doesn’t diagnose chronic diastolic dysfunction—it estimates real-time LAP * E/e’ ≥ 14 supports elevated LAP and cardiogenic pulmonary edema physiology * E/e’ ≤ 8 makes elevated LAP less likely—pursue alternative causes of dyspnea * With a decent apical view, E and e’ are obtainable fast * The right call can be diuretics instead of antibiotics*, and a better trajectory for your patient Clinical Bottom LineWhen you suspect pulmonary edema, don’t stop at lung ultrasound or BNP. Reach for your apical view, capture E and e’, and ask the real question:

Is the left atrial pressure elevated enough to flood the lungs?With POCUS diastology, you’ll have the answer in under 60 seconds.

References1. Greenstein YY, Mayo PH. Evaluation of Left Ventricular Diastolic Function by the Intensivist. Chest. 2018;153(3):723-732. PMID: 29113815 2. Del Rios et al. Emergency physicians used average e’ (<9 cm/s) alone to assess for diastolic dysfunction. Compared to cardiology standard, agreement was 85.4% (κ = 0.74). Shows the feasibility of streamlined approaches in real ED practice. J Ultrasound Med. 2018 May;37(5):1237-1243 3. ASE/EACVI 2025 Guidelines – The most recent comprehensive guidance on echocardiographic assessment of diastolic function, re-emphasizing the centrality of E/e’ in estimating LAP. J Am Soc Echocardiogr. 2025 Apr;38(4):278-317 Post Peer Reviewed By: Marco Propersi, DO (X: @Marco_propersi), Mark Ramzy, DO (X/IG: @MRamzyDO), Jailyn Avilla, MD (Insta: @jailyn_avi)

Guest Authors Joseph Felice MD FPD-AEMUSAPD, Ultrasound DivisionVassar Brothers HospitalPoughkeepsie, New York Neha Kumrah, DOPGY 1 Emergency Medicine ResidentVassar Brothers HospitalPoughkeepsie, New YorkShowing Slide 1 of 2 Your Deep-Dive Starts Here###### Diastology: Use E/e’ to Estimate Left Atrial Pressure

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CardiovascularRead MoreShowing Slide 1 of 4The post Diastology: Use E/e’ to Estimate Left Atrial Pressure appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL RundownKey Points Try the coffee nap! Where you combine caffeine and a 30-minute nap to then have that boost energy and alertness by the time it kicks in.

Sleep isn’t optional—it’s crucial for memory, mood regulation, and physical recovery. It is fundamentally different from rest

Replacing sleep with caffeine isn’t effective and can have negative health impacts. Make getting enough sleep a priority

Sunlight exposure is important for maintaining circadian rhythms and sleep quality. This applies even if you work as a nocturnist

Creating a personalized sleep system enhances quality and consistency. It gives you back control of a schedule that you may feel like is out of your hands.

If you’ve tried these strategies and you’re still struggling, consider true sleep pathology (insomnia, shift work disorder, sleep apnea) and get help—this is not a “be tougher” problem.

Better sleep isn’t just about feeling good; it’s directly tied to error reduction, patient safety, and longevity in EM/ICU careers.

Click here for Direct Download of the Podcast.

Previously Covered and Related Content: + REBEL Core Cast: Sleep Hygiene + REBEL MIND: Rest Is Not Sleep: The Seven Dimensions of True Recovery + Rebellion in EM: Care For Yourself – Sleep Hygiene + First10EM: Some Evidence For Working Night Shifts + REBEL MIND: Dunning Kruger Effect IntroductionWelcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during D*ifficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine.

Today we are exploring the imperative topic of rest and why it’s not just about sleeping. The second of a two part series, hosted by Dr. Mark Ramzy with guests Dr. Maureen Aiad and Dr. Amil Badoolah, continue our discussion but this time on the multifaceted nature of sleep, how it serves as medicine and how we can use our tools deliberately to get more of it!

Cognitive QuestionHow would your clinical performance, patience with families, and long-term career sustainability change if you treated sleep as a non-negotiable clinical intervention rather than a flexible “nice-to-have”?

How is Sleep Different From Rest?1. Rest reduces load; sleep repairs systems

• • We previously talked about the 7 types of rest and you can check that out here
  • Examples of physical rest include: pausing tasks, stepping away from the monitor, taking a walk, stretching, breathing, journaling, connecting with a colleague. This lightens your cognitive/emotional burden.

  • Sleep is fundamentally different in that it’s an active biologic process that helps:

    • • Consolidates memory and learning (yes, including the tough cases from last night).
      • Regulates mood, impulse control, and emotional reactivity.
      • Supports immunity, metabolic health, and cardiovascular function.
      • Repairs tissue, replenishes neurotransmitters, and fine-tunes neural networks.
      • You can have “rested but underslept” days (you took breaks but got 4 hours in bed), and “slept but unrested” days (you got hours, but all junk sleep). Both matter, but they are not interchangeable.

2. Sleep architecture vs. “knocking out”

• • True restorative sleep cycles through NREM and REM in predictable patterns.

  • Alcohol, late caffeine, and fragmented nights may help you fall asleep faster but:

    • Suppress REM.
    • Shorten deep sleep.
    • Increase awakenings and light sleep.
      • The result: you technically slept, but your brain didn’t get the “software updates” it needed.

Biology isn’t built for your schedule

• • Circadian rhythms were designed for light-day / dark-night cycles, not: - 10 pm–7 am ED shifts. - 24-hour calls. - 6 nights in a row followed by days.
  • Your body can adapt partially, but not instantly and not perfectly. That’s why:
    • You can feel “jet-lagged” even when you haven’t traveled.
    • Sleep before and after nights feels odd and fragile.
• Recognizing that “this is biologically unnatural” is key: you’re not weak; you’re fighting physiology. How This Applies to the Emergency Department or ICU?1. Performance & safety
  • Sleep deprivation:
    • Slows reaction time and increases error rate.
    • Impairs risk assessment and complex decision-making.
    • Drops your frustration tolerance with consultants, families, and staff.
  • In both emergency medicine and critical care, that translates into:
    • Anchoring on the wrong diagnosis.
    • Missing subtle clinical changes.
    • Snapping at a tech, nurse or resident and damaging team culture.
• Chronic health for chronic shift workLong-term sleep disruption is associated with:
  • Hypertension, diabetes, obesity.
  • Depression, anxiety, burnout.
  • Arrhythmias (e.g., AFib) and increased stroke risk.
  • Possibly increased all-cause mortality.You’re already in a high-stress, high-exposure specialty. Chronically poor sleep amplifies that risk profile and can end a career early—or make you miserable while you’re still in it.

• Culture of “heroics” vs. health

  • Skipping sleep to pick up extra shifts, late meetings, or “just one more note” is often praised.

  • We rarely celebrate:

    • The attending who says “no” to a 2 pm meeting post-nights.

    • The resident who defends their blackout-curtains-and-earplugs routine. Different Ways to Improve Your Sleep + Clarify your “sleep non-negotiables”*

    • Decide how many hours you realistically need to function (e.g., 7–9 on off days, realistic blocks on nights).

    • Treat those hours as you would a procedure time—blocked, protected, and respected.Use caffeine like a drug, not a reflex

    • Aim for ≤ 2 cups equivalent on most days.

    • Avoid caffeine within 4–6 hours of your planned sleep time (remember: it can hang around up to 12 hours).

    • Consider scheduling caffeine for:

      • Early in the shift for alertness.
      • Strategic “coffee naps” (see below), not late-night chugging.Respect alcohol’s impact on sleep

    • Recognize that even small to moderate doses degrade sleep architecture.

    • Avoid using alcohol as a “sleep aid”—you’ll fall asleep faster but sleep worse.

    • If you do drink, separate it from bedtime and keep it modest.Optimize food and fluid timing

    • Hydrate consistently on shift, but taper fluids ~4 hours before bed to reduce nocturnal bathroom trips.

    • Avoid heavy, spicy, or large meals within 2–3 hours of sleep to decrease reflux and discomfort.

    • Plan a light, balanced “pre-sleep” snack if going to bed hungry keeps you awake.Move your body (but not right before bed)

    • Regular exercise improves sleep depth and latency.

    • Try to avoid intense workouts within 2 hours of bedtime.

    • On shift: micro-movement (stairs, brisk walks between pods, quick stretch sessions) can help alertness without wrecking sleep later.Control light exposure

    • Maximize sunlight or bright light after waking (even if that’s 3–4 pm after a night).

    • Minimize bright light and screens before sleep:
      • Dim lights.
      • Use night mode/blue-light filters if you must scroll.

    • For daytime sleep:

      • Use blackout curtains, tinfoil, cardboard, or sleep masks.
        • Yes seriously use tinfoil if you have to, we talk about it on the podcast episode!
      • Aim for “I might be blind” darkness—so dark you can’t see your hand in front of your face.Dial in your sleep environment

    • Cool room temperature (fan or AC if possible).

    • White noise or sound machine to mask household/traffic noise.
    • Earplugs and eye masks as needed.

    • Bed used primarily for sleep (and sex)—not for charting, doom scrolling, or email.Strategic power naps

    • Keep naps ≤ 20–30 minutes to avoid sleep inertia.

    • Prefer early-afternoon or pre-night-shift naps.

    • Coffee nap strategy:

      • Drink a small coffee.
      • Immediately lie down for a 20–30 min nap.
      • Wake up as the caffeine kicks in, combining nap benefit + stimulant.Thoughtful melatonin use

    • Remember melatonin is a hormone, not a vitamin gummy.

    • Lower doses often work as well as (or better than) large OTC doses.
    • Use it intentionally and intermittently, not as a crutch every night.

    • Over-reliance may reduce your own natural production and its effectiveness over time.Build pre-sleep rituals

    • Repeated, calming habits signal your body it’s time to downshift:

      • Warm shower, gentle stretching, or yoga.
      • Guided breathing or body scan.
      • Brief journaling or “brain dump” of tasks to get them out of your head and onto paper.Protect from pathologic patterns

    • If despite consistent effort you:

      • Snore heavily, stop breathing, or gasp in sleep.
      • Feel excessively sleepy driving home or at work.
      • Cannot fall asleep or stay asleep for weeks to months.Consider evaluation for sleep apnea, insomnia, or shift-work sleep disorder with your physician or sleep specialist. Immediate Action Steps for Before/During/After Your Next Shift1. Before the Shift:
• • Plan a 20–90 minute nap before your first night shift (many clinicians find 3–5 hours earlier in the day is ideal). - I treat ED and ICU shifts very differently. I always sleep 3-5 hours before my night shifts aiming for the full 5 (sometimes 6 or more) hours for my ED shifts because you always have to be “on”. Depending on the ICU I’m working in, I may have a bit more downtime so 3 to 5 hours is plenty.
  • Set a caffeine plan: decide in advance when your last dose will be (e.g., none after 2–3 am if sleeping at 8–9 am).
  • Tell your household, “This is my sleep block” and agree on a plan for kids, pets, deliveries, etc.

• On my calendar, I completely block off time called “Pre-call sleep” so no meetings can be scheduled and then put my phone in airplane mode

• During the Shift

• • Hydrate early; taper fluids in the last 3–4 hours of your shift
  • Eat something light but adequate; avoid “last-minute” heavy meals right before sign-out.
  • Build in micro-breaks and movement: one or two short walks, a few stretches, even a quick stair run if safe.
  • Get outside or near a window for a few minutes of light exposure if possible.

• After the Shift

• • On the way home: - Use sunglasses to reduce bright morning light if you’re aiming for sleep soon. - Avoid “just checking” email or messages; shift into wind-down mode.
  • At home:
    • Do a brief, calming decompression (shower, light snack, 10–15 minutes of low-stimulation TV or reading).
    • Make your room cold, quiet, and dark (blackout curtains, tinfoil/cardboard, white noise, fan).
    • Put your phone on Do Not Disturb and physically place it away from the bed.
      • On my calendar, I completely block off time called “Post-call sleep” so again no meetings can be scheduled and then I personally don’t just put my phone on Do Not Disturb but rather in airplane mode and WIFI OFF
  • If you can’t sleep after ~20–30 minutes:
    • Get out of bed, do something calming in dim light (breathing, gentle stretching, journaling).
    • Return to bed when sleepy—this trains your brain to associate bed with sleep, not frustration. ConclusionRest and sleep are both critical—but they’re not interchangeable. Rest helps you step out of the constant “on” of our jobs, while sleep is the biological intervention that restores your ability to show up safely and sustainably. Rest ≠ sleep. Rest reduces load; sleep repairs your brain and body. You need both, on purpose.

As EM and ICU clinicians, we’re trying to perform formula-one-level medicine with engines that often only see half their maintenance. You won’t fix shift work. You can build a sleep system that respects your biology, your schedule, and your life at home.

That system starts with valuing sleep, then prioritizing it, personalizing it, trusting the process when it’s imperfect, and actively protecting both your routine and your mindset.

Clinical Bottom LineSleep is medicine. Shift work is biologically unnatural. Struggling does not mean you’re weak; it means you’re human fighting physiology. Use your tools deliberately. Caffeine, naps, light, food, movement, melatonin, and environment can be leveraged—or can quietly sabotage you. Build and defend a personalized sleep routine. Communicate it, normalize it, and protect it from casual encroachment. You can’t control every trauma, code, or admission—but you can control how seriously you take your own recovery. Your patients, your team, and your future self all benefit when you do.

Further Reading1. Espie CA.
The ‘5 principles’ of good sleep health. J Sleep Res. 2022 Jun;
PMID: 34676592 2. Solodar, J“Sleep hygiene: Simple practices for better rest.” Harvard Health, 31 January 2025
Link is Here 3. Suni, E.

“Mastering Sleep Hygiene: Your Path to Quality Sleep.” Sleep Foundation, 7 July 2025,
Link is Here Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ * * Maureen Aiad, DOAssistant Professor of Emergency MedicineNYU Grossman Long Island School of Medicine, New York * Amil Badoolah, DOAssistant Professor of Emergency MedicineNYU Grossman Long Island School of Medicine, New YorkShowing Slide 1 of 3###### REBEL Core Cast 119.0 – Sleep Hygiene

REBEL Core Cast 119.0 – Sleep Hygiene Click here for Direct Download of ...

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REBEL Rundown Key Points Understanding the Why: The significance of understanding underlying causes, beyond initial diagnoses, in both sports and emergency medicine is explored.
Recovery Focus: Emphasizing the importance of recovery time and small daily choices in optimizing performance for both athletes and emergency physicians.
Data-Driven Insights: The Arena Labs approach uses personalized data, leveraging wearable technology and expert coaching to tackle burnout and enhance well-being.
Personalization and Partnership: Arena Labs’ collaboration with emergency clinicians sheds light on personalized performance solutions rooted in scientific evidence.

Click here for Direct Download of the Podcast.

IntroductionWelcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, we’re excited to continue collaboration with Arena Labs, where host Dr. Mark Ramzy interviews Allyn Abadie, Arena Labs’ Principal Scientist on how we can apply performance science in and out of the emergency department. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.

Previously Covered on REBEL MIND: Performance Under Pressure – What Medicine Can Learn from Elite Teams * The Power of Performance Coaching in Medicine * Rest Is Not Sleep: The Seven Dimensions of True Recovery Cognitive QuestionHow can emergency department clinicians utilize techniques inspired by athletic performance to better manage stress, prevent burnout, and optimize recovery?*

Why This is Important + Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals. How This Applies to the Emergency Department or ICU? + Emergency medicine, akin to high-performance sports, demands intense energy and quick decision-making under pressure, often leading to stress and burnout. By applying principles from athletic recovery and personalized data tracking, clinicians can moderate their performance intensity, enhance their recovery even in short breaks, and prevent long-term burnout. This approach allows emergency physicians to maintain endurance and clarity, improving patient care and team dynamics. Things You Can Do on Your Next Shift + Measure and Reflect: Start tracking your vital health metrics like heart rate with wearable sensors. Reflect on how daily activities impact these measurements to identify stress patterns. + Implement Quick Recovery Techniques: Use short, actionable exercises such as deep breathing or the de-stress breath method between patient encounters to moderate stress levels. + Invest in Self-Care: Dedicate brief time slots for essential self-care activities like hydration or quick reflection journaling, aiming to enhance mental resilience throughout your shift. + Utilize Coaching Tools:* Engage with personalized coaching apps or resources that offer science-backed recovery strategies tailored to your personal and professional needs. Where to Learn MoreIntrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance.

Clinical Bottom LineIn an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine.

Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for.

Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefRWJBH / Rutgers Health, Newark NJ* * Allyn AbadiePrincipal ScientistArena LabsShowing Slide 1 of 2###### REBEL MIND – Teaching Towards Expertise with Gamification

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Human BehaviorRead More###### REBEL MIND – The Mental Jump: Moving from Junior to Senior Leadership in Emergency Care

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REBEL Rundown Key PointsThe 4 Steps of an ED Consult:

1. Introduce yourself and your role
2. Lead with the outcome (the ask)
3. Give a focused case summary (why it’s theirs + what you’ve done)
4. Close the loop (timeline, next steps, contingencies) Click here for Direct Download of the Podcast.

IntroductionToday we’re tackling one of the most important (and most under-taught) skills in emergency medicine: how to call a consult in the ED and what to do when a consultant pushes back.

To call a consult in the ED, start with a brief introduction, lead with the outcome you need (“the ask”), give a focused decision-relevant summary, and close the loop with timeline and next steps. If the consultant resists, clarify the “why,” restate the ask, offer alternatives, and escalate when patient safety or disposition is at risk.

After two decades in emergency medicine and countless consult calls, here’s a simple framework—plus copy/paste scripts—to make your consults faster, clearer, and easier to say “yes” to.

Why Consult Skills Matter in Emergency Medicine Consults aren’t a formality—they’re a patient-care intervention. Strong consult communication:* + Reduces delays in time-sensitive care + Improves ED throughput and disposition + Decreases conflict and miscommunication + Clarifies ownership and next steps + Protects the patient (and the team) when plans are unclear The 4-Step ED Consult Framework (Introduction → Ask → Summary → Close the Loop)Most consult friction comes from one of two problems: unclear expectations or excessive noise. This four-step structure solves both.

1) Introduce yourself and your roleA simple intro sets a professional tone and removes ambiguity.

Script:

“Hey, this is Swami, one of the ED attendings. I’m calling for an ortho consult.”

2) Lead with the outcome (the ask)Don’t bury the lede. The consultant wants to know what you need—immediately.

Script:

“I’m calling about a patient with a suspected septic knee. I need you to evaluate for operative management.”

3) Give a focused, decision-relevant summaryYour summary should answer:

• Why this is your service’s problem
• What’s already been done
• What I’m worried about / what decision is needed now

Script:

“43-year-old man with no major PMH, 3 days of knee pain and swelling. XR negative. Febrile. Aspiration yielded purulent fluid—cultures sent. We started antibiotics after the tap. He’s hemodynamically stable.”

High-yield pearl: Add quick “stability anchors” when relevant:

• “Airway stable, pain controlled.”
• “Neurovascularly intact.”
• “No signs of compartment syndrome.”
• “No hypotension or escalating oxygen requirement.” 4) Close the loop (timeline + next steps)This prevents the consult from floating in limbo and protects patient flow.

Script:

“When do you expect to see the patient, and do you want anything done before you arrive—NPO, repeat labs, additional imaging?”

ED Consult ScriptGeneral ED Consult Script

“Hi, this is Dr. ___ in the ED. I’m calling for a ___ consult. The reason is ___. Briefly: ___ year-old with ___. We’ve done ___ and started ___. I’m concerned about ___. Can you see them today, and what’s your preferred next step?”

Septic joint / Ortho Example

“Hi, this is Swami in the ED. I need an ortho consult for suspected septic arthritis. 43-year-old with 3 days of atraumatic knee swelling and fever. XR negative. Tap produced purulent fluid—cultures sent. Antibiotics started after aspiration. Can you evaluate for operative management, and when can you see the patient?”

Neurology example (time-sensitive)

“Hi, this is Dr. ___ in the ED. I need neurology for suspected acute stroke. Last known well ___. NIHSS ___. CT/CTA completed (or pending). I’m calling to discuss candidacy for thrombolysis/thrombectomy and next steps. When can you evaluate and what additional workup do you want now?”

Common ED Consult Mistakes (and Fixes)Mistake: Long story before the ask

Fix: Lead with the outcome in the first sentence

Mistake: Unfiltered data dump

Fix: Provide only decision-relevant details

Mistake: No timeline

Fix: Ask explicitly when they’ll see the patient and what they need first

Mistake: Implicit “ownership”

Fix: Clarify who is admitting, who is following, and what happens if the patient worsens

What to Do When a Consultant Pushes BackEven a perfect consult can meet resistance. Your job is to stay calm, keep it professional, and protect the patient.

1) Ask “why?”Don’t argue first—diagnose the refusal.

Script:

“Help me understand your concern about seeing this patient.”

Many refusals are based on misunderstanding: wrong service, missing key detail, or incorrect assumption about stability.

2) Restate the consult in one sentence, then offer optionsIf the conversation starts spiraling, reset it.

Script:

“To be clear, I’m concerned this is septic arthritis and needs ortho evaluation. If you don’t feel you’re the right service, who should be—rheum, medicine, or another surgical team?”

This keeps you collaborative while preventing dead ends.

3) Humanize the decision (use sparingly)This is a “high-voltage” tool. Use it when stakes are high and you’ve already clarified the medical facts.

Script:

“I’m worried we’re missing something time-sensitive. If this were your family member, what would you want us to do next?”

Use it to re-anchor to patient risk—not as a guilt tactic.

When and How to Escalate a ConsultEscalation isn’t personal—it’s a safety mechanism when there’s an impasse that threatens timely care.

When to escalate Time-sensitive condition is delayed (e.g., septic joint, cord compression, testicular torsion, GI bleed with instability) * No clear disposition plan despite reasonable ED evaluation * Consultant refusal blocks needed specialty decision-making * Patient safety or deterioration risk is increasing in the ED How to escalate (lowest to highest intensity)*1. Ask for the consultant’s attending (if speaking to a resident) 2. Call the on-call attending directly 3. Involve ED leadership/medical director 4. Escalate to service chief/department chair (rare, but real) 5. Hospital supervisor/admin escalation for immediate operational impasse

Script:

“We’re at an impasse and the patient needs a decision. I’m escalating to clarify ownership and ensure timely care.”

Documentation Tips for Consult RefusalsDocumentation should be factual and patient-centered, not punitive.

Include:

• Your clinical concern and why the consult is needed
• Who you spoke with (name/role)
• Their stated reason for refusal or delay
• Alternatives discussed
• Escalation steps taken and final plan FAQ: Emergency Medicine ConsultsWhat is the best way to call a consult in the ED?Introduce yourself, lead with the specific ask, summarize only decision-relevant details, and close the loop with a clear plan and timeline.

What should I say when a consultant refuses to see a patient?Ask why, clarify misunderstandings, restate your concern and the ask, and request an alternative plan or appropriate service.

When should I escalate a consult?Escalate when an impasse delays time-sensitive care, threatens patient safety, or prevents appropriate disposition.

How do I document a refused consult?Document the clinical concern, who you spoke with, their stated reason, alternatives discussed, and escalation steps taken.

ConclusionMastering emergency medicine consults makes you faster, safer, and easier to work with. The goal isn’t to “win” a consult call—it’s to get the patient the right care, with clear ownership and a shared plan.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Associate Editor###### Anand Swaminathan

MD, MPHAll Things REBEL EM

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REBEL Rundown Key Points HFNC met criteria for non-inferiority to BPAP for preventing intubation or death within 7 days in four of the five ARF subgroups. * Bayesian dynamic borrowing increased power across subgroups but created variable certainty, especially in smaller groups such as COPD. * The immunocompromised hypoxemia subgroup did not meet non-inferiority, leading to early trial stopping for futility. * Rescue BPAP use*, subgroup-specific exclusion criteria, and non-standardized BPAP delivery are important contextual factors that influence how subgroup results should be interpreted. Click here for Direct Download of the Podcast.

Introduction Bilevel Positive Airway Pressure (BPAP) has long been a foundational modality in the management of acute respiratory failure (ARF), particularly in COPD exacerbations and cardiogenic pulmonary edema, where it can rapidly reduce work of breathing and improve gas exchange. It remains a core tool in our respiratory support arsenal. * High-flow nasal cannula (HFNC), however, has expanded what we can offer patients by delivering many of the same physiologic benefits through a far more comfortable interface. With high flows, modest PEEP, and effective dead-space washout, HFNC can improve oxygenation and decrease work of breathing while preserving the ability to talk, cough, eat, and interact with staff and family. This combination of physiologic support and tolerability makes HFNC especially attractive in patients where comfort, anxiety, or cardiovascular stability are key considerations, and in settings where prolonged noninvasive support may be needed. Rather than competing with BPAP, HFNC broadens our options in ARF and allows us to better match the modality to the patient and their underlying disease process. * The RENOVATE trial set out to answer a high-impact question across five distinct etiologic groups: Is HFNC non-inferior to BPAP (NIV) for preventing intubation or death in acute respiratory failure? PaperAzoulay É, et al. High-Flow Nasal Oxygen vs Noninvasive Ventilation in Patients With Acute Respiratory Failure: The RENOVATE Randomized Clinical Trial. JAMA*. 2025 PMID: 39657981

Previously Covered On REBEL: HFNC: Part 1 – How It Works * HFNC: Part 2 – Adult and Pediatric Indications * FLORALI and AVOID Trial * FLORALI-2: NIV vs HFNC as Pre-Oxygenation Prior to Intubation * The Pre-AeRATE Trial – HFNC vs NC for RSI* What They DidCLINICAL QUESTIONIs HFNC non-inferior to BPAP for rate of endotracheal intubation or death at 7 days in patients with acute respiratory failure due to a variety of causes?

STUDY DESIGN Multicenter, randomized non-inferiority trial * 33 Brazilian hospitals * Nov 2019 – Nov 2023 * Adaptive Bayesian hierarchical modeling with dynamic borrowing * Open label, outcome adjudicators blinded * Patients were classified into 5 subgroups SUBGROUPS1. Non-immunocompromised hypoxemia*

• SpO₂ < 90% on room air or
• PaO₂ < 60 mm Hg on room air plus
  • Increased respiratory effort (accessory muscle use, paradoxical breathing, thoracoabdominal asynchrony) or
  • Respiratory rate > 25 breaths/min

2. Immunocompromised hypoxemia

Defined as:

• • Use of immunosuppressive drugs for >3 months
  • OR high-dose steroids >0.5 mg/kg/day
  • OR solid organ transplant
  • OR solid tumors or hematologic malignancies (past 5 years)
  • OR HIV with AIDS / primary immunodeficiency

3. COPD exacerbation with acidosis

• High clinical suspicion of COPD as primary diagnosis
• RR >25 with accessory muscle use, paradoxical breathing, and/or thoracoabdominal asynchrony
• ABG: pH <7.35 AND PaCO₂ >45

4. Acute cardiogenic pulmonary edema (ACPE)

• Sudden onset dyspnea and rales
• ± S3 heart sound
• No evidence of aspiration, infection, or pulmonary fibrosis
• CXR consistent with pulmonary edema

5. Hypoxemic COVID-19 (added June 2023)

• Added due to deviations between expected and observed outcome proportions
• Any patient across the other 4 groups with PCR-confirmed SARS-CoV-2 infection in any of the above groups POPULATION

| Inclusion Criteria: ≥18 yrs with ARF in one of 5 pre-defined subgroups excluding COPD was defined by the following:Hypoxemia with SpO₂ <90 or PaO₂ <60 * Accessory muscle use, paradoxical breathing, and/or thoracoabdominal asynchrony * RR >25 BPM | Exclusion Criteria:* Need for emergency intubation * Prolonged apneic episodes * Cardiorespiratory arrest * GCS <12 * HR <50 with decreased consciousness * ABG pH <7.15 * Severe agitation requiring heavy sedation * Hemodynamic instability (MAP <65, SBP <90 despite fluids or requiring high-dose pressors) * Contraindications to BPAP (facial trauma, recent esophageal surgery, copious secretions, vomiting, aspiration risk) * Pneumothorax or large pleural effusion * Severe arrhythmia * Thoracic trauma as primary ARF cause * Asthma attack * Cardiogenic shock * ACS requiring urgent cath * ARF within 72h post-extubation * Post-surgical ARF within 72h * Hypercapnic ARF due to neuromuscular/chest wall disease * Palliative care or DNI * Chronic pulmonary disease other than COPD * 6 hours BPAP prior to randomization (hypoxemic non-immunocompromised, immunocompromised, and COPD groups) * Prior BPAP use in ACPE |

INTERVENTION & COMPARATOR

| Intervention (HFNC Group): Flow: + COPD: Start 30 L/min + All others: Start 45 L/min + Titrated up to 60 L/min or highest tolerated * FiO₂: + Start at 50% and titrate to maintain target SpO₂ * SpO₂ Targets: + COPD: 88–92% + Others: 92–98% * Rescue Therapy (COPD & ACPE only): + If failing maximal HFNC → 1 hour of rescue BPAP + If failing BPAP → immediate intubation * Weaning + Begin ≥24 hrs once RR <25 and no distress + Gradual reductions in FiO₂/flow + Considered weaned at: - FiO₂ <30% and Flow <25–30 L/min | Comparator (BPAP Group):** Via ICU ventilator or BiLevel device * Initial Settings: + COPD: IPAP 12–16 / EPAP 4 + Others: IPAP 12–14 / EPAP 8 * Max settings: IPAP 20 / EPAP 12 * SpO₂ Targets: + COPD: 88–92% + Others: 92–98% * Titration: Not standardized * Sedation: Not standardized * Weaning: + After 24 hrs + At clinician discretion + Considered weaned at FiO₂ 30% and EPAP/PS <6 |

OUTCOMES

| Primary Outcome: Endotracheal intubation or death within 7 days. | Secondary Outcomes: 28-day mortality * 90-day mortality * Mechanical ventilation free days at 28 days * ICU-free days at 28 days | Tertiary Outcomes:*** Hospital and ICU length of stay within 90 days * Vasopressor-free days within 28 days * New DNI orders within 7 days * Patient comfort |

Results: Critical ResultsMOR: Median Odds Ratio
MHR: Median Hazard Ratio

Strengths Broad, multicenter design: Large multicenter randomized trial comparing HFNC vs BPAP across several etiologies of acute respiratory failure in ED and ICU settings. * Etiology-based and COVID-specific subgroups: Patients were stratified into prespecified clinical subgroups (COPD with acidosis, ACPE, immunocompromised hypoxemia, non-immunocompromised hypoxemia), and COVID-19 was later added and analyzed as a separate subgroup rather than being combined with the original ARF categories. * Bayesian hierarchical model with dynamic borrowing: The primary analysis used a Bayesian hierarchical framework that allowed information to be borrowed across subgroups when treatment effects were similar and reduced borrowing when subgroups differed. * Prespecified non-inferiority and futility rules: Each subgroup had predefined non-inferiority and futility boundaries, and enrollment in the immunocompromised subgroup was stopped early after crossing a futility threshold. * Standardized BPAP delivery system: BPAP was delivered using a single BPAP system/interface across participating centers. * Single healthcare system and population: All sites were within one national healthcare system, with broadly similar clinician training, practice patterns, and patient populations for that country. * Current practice relevance: The trial addresses a post-COVID era question in which HFNC is widely used, providing comparative HFNC vs BPAP data across multiple ARF etiologies in a pragmatic ED/ICU population. Limitations Small subgroup sizes: The COPD (35 vs 42) and immunocompromised (28 vs 22) subgroups included relatively few patients compared with the other etiologic groups. * Dependence on borrowing for COPD estimates: COPD treatment-effect estimates in the primary model were heavily influenced by borrowing from other subgroups, and no-borrowing sensitivity analyses showed wider intervals. * Pre-randomization BPAP and exclusion criteria: COPD patients could receive up to 6 hours of BPAP before randomization, and ACPE patients judged to require immediate BPAP were excluded from enrollment. * Rescue BPAP in the HFNC arm: Patients assigned to HFNC could receive rescue BPAP; BPAP settings were not standardized, and detailed reporting of rescue BPAP management and outcomes (including number of episodes) was limited. * Non-standardized weaning strategies: Weaning protocols for HFNC and BPAP were not tightly protocolized or aligned, and HFNC weaning permitted flows down to 25–30 L/min. * Single-country setting: All participating centers were located in one country. Side Tangent on Bayesian Adaptive Model Prior to our deep dive into the discussion, lets first explain the importance of the statistical method used in the RENOVATE trial, the Bayesian Adaptive Model. * A Bayesian Adaptive Model is a trial design that keeps updating its understanding of which treatment works better as new data are collected, and it allows the trial to change course in real time based on those results. * Now imagine you’re comparing two pairs of running shoes. Your goal is to see which one helps runners finish faster, so you measure their race times. Runners try Shoe A or Shoe B, and as the results come in, you analyze the times. * + If runners wearing Shoe A and Shoe B are finishing within a few seconds of each other, you would conclude the shoes perform similarly, meaning they are non-inferior. + If runners wearing one shoe are consistently finishing much faster, you can say that shoe is superior, and the trial may stop early because you’ve clearly found the better option. + If one shoe repeatedly produces slower times compared to the standard, you may stop the trial for inferiority, because continuing would not benefit runners. * This approach allows the study to learn as it goes and make decisions based on accumulating evidence rather than waiting until the very end. * The Bayesian adaptive model also utilizes a statistical tool known as dynamic borrowing. Dynamic borrowing is a statistical method that allows data from related groups to be shared or pooled when their outcomes appear similar, but automatically reduces or stops that sharing when the groups differ, ensuring accuracy and preventing misleading conclusions. * For example, if Shoes A and B are producing similar race times (non-inferior), the coach can combine or “borrow” data from both groups and average their times, which increases statistical precision. * However, if one shoe becomes clearly superior or clearly inferior, dynamic borrowing stops, because the race times are no longer comparable and averaging them would distort the results. * In this running-shoe analogy, the RENOVATE trial was essentially comparing Shoe A (BPAP) and Shoe B (HFNC) to see which helped patients “run faster,” or achieve better clinical outcomes in 5 different pathologies. * In this running-shoe analogy, the RENOVATE trial was essentially comparing Shoe A (BPAP) and Shoe B (HFNC) to see which helped patients “run faster,” or achieve better clinical outcomes across five different respiratory pathologies. As results accumulated, the Bayesian adaptive model used dynamic borrowing and could combine results when both devices performed similarly, but stopped pooling data if one clearly helped patients more or less. Discussion What RENOVATE asked and what it found: The RENOVATE trial is the first multicenter randomized study to directly evaluate whether HFNC is non-inferior to BPAP for preventing intubation or death across multiple etiologies of acute respiratory failure. Overall, HFNC met non-inferiority criteria in four of the five predefined subgroups, with much of the statistical strength coming from the Bayesian borrowing structure. However, several design and analytic choices limit how confident we can be in these findings across all groups. * Bayesian model, borrowing, and small numbers: The Bayesian hierarchical model improves precision by “sharing” information between subgroups when outcomes look similar, but this does not fully fix the problem of small sample sizes. In subgroups with low numbers, the model still has less power and more uncertainty, and the apparent stability of the estimates is heavily influenced by the borrowing framework rather than large, subgroup-specific datasets. * COPD and ACPE – who actually got randomized: In both COPD and ACPE, enrollment decisions likely removed many of the sickest patients from randomization. COPD patients could be stabilized for up to six hours on BPAP before being randomized, and ACPE patients who clearly required immediate BPAP were excluded altogether. Because the trial never reported how many patients were treated or excluded in the ACPE group, we do not have a clear picture of how sick the randomized patients really were. * Rescue BPAP in the HFNC arm: Rescue therapy adds another layer of ambiguity. Nearly a quarter of COPD patients in the HFNC arm required rescue BPAP, yet the study did not describe the BPAP pressure settings used, how many times rescue could be repeated, or whether these patients ultimately improved, failed, or required intubation. This is particularly important because the primary endpoint is intubation within seven days, and we do not know how much non-standardized BPAP rescue influenced that outcome in patients initially assigned to HFNC. * Different weaning strategies between HFNC and BPAP: Weaning practices also differed meaningfully between HFNC and BPAP. HFNC patients could be considered “weaned” while still receiving flows that are well above physiologic baseline (25–30 L/min), whereas BPAP weaning was left largely to clinician judgment without tightly aligned criteria. This lack of standardized weaning makes it difficult to directly compare the two modalities in terms of duration of support and when a treatment should be considered to have “failed.” * Value of multiple etiologic subgroups: Rather than asking a single global question of whether HFNC works for all causes of acute respiratory failure, the trial was designed with multiple etiologic subgroups. This allows us to compare HFNC and BPAP within distinct pathologies commonly seen in the ED and ICU. In practice, this design helps us look across each subgroup and think about which modality—HFNC or BPAP—may be most appropriate for a given underlying diagnosis. * Immunocompromised subgroup had early futility and inadequate support: In immunocompromised patients, HFNC clearly underperformed BPAP on early outcomes. Intubation rates were higher with HFNC (50.0% vs 31.8%), and early deaths were also higher (17.9% vs 13.6%), leading this subgroup to cross a prespecified futility boundary and stopping further enrollment. By 28 and 90 days, mortality was similar between HFNC and BPAP in this cohort, suggesting that HFNC alone did not provide enough up-front respiratory support for this high-risk group rather than causing a lasting difference in long-term outcomes. * Why COVID was separated from the original ARF subgroups: Early in the COVID-19 pandemic, clinicians were making treatment decisions in real time without established guidelines or a solid understanding of disease trajectory. Many COVID patients behaved clinically like an immunocompromised or atypical ARF cohort. If COVID patients had been left inside the original ARF subgroups, they could have distorted those results and biased the trial toward an apparent signal of HFNC futility. By separating COVID into its own subgroup, the investigators preserved the integrity of the non-COVID etiologic groups while still including COVID patients in the overall study population. This approach allowed for cleaner estimates within each subgroup and more appropriate borrowing across groups without letting a large, atypical population dominate the model. * Standardized BPAP delivery as a control: Using one BPAP delivery method for all patients created a built-in control on the BPAP side of the trial. The interface and mode were standardized, so the main difference between patients was their underlying disease and assignment to HFNC vs BPAP. This consistency across BPAP subgroups reduces “noise” in how BPAP was delivered and makes it easier to attribute differences in outcomes to the disease process and modality choice rather than variation in the BPAP setup itself. * Single-country setting and external validity: Running the entire study in one country means clinicians share similar training, practice patterns, and system-level resources, which helps keep management more consistent across subgroups and centers. The trade-off is external validity: what is considered “standard” care in this health system may look very different in other countries, particularly in resource-limited settings, so these findings may not translate perfectly to other practice environments. Author's Conclusion“HFNC met criteria for noninferiority to NIV for the primary outcome in 4 of the 5 patient groups. Small sample sizes and sensitivity to the analysis model suggest further study is needed in COPD, immunocompromised patients, and ACPE.”

Our ConclusionHFNC appears to perform comparably to BPAP in non-immunocompromised hypoxemic and COVID-positive patients. However, the data in COPD, ACPE, and immunocompromised patients are limited and statistically fragile—heavily influenced by small numbers and modeling assumptions—so BPAP should remain the preferred modality when ventilatory support is clearly required and may offer more reliable benefit in these groups.

Clinical Bottom LineHFNC is a great option for many patients with acute respiratory failure, but some patients clearly need BPAP up front. In patients with obvious BPAP-responsive physiology—such as COPD with acidosis, ACPE with increased work of breathing, or frank hypercapnia—or in those who are crashing at the door, BPAP remains the first-line choice. In more stable patients, especially those without a strong indication for BPAP, with limited hypercapnia, or where comfort and longer-term tolerance matter, HFNC is a reasonable first-line option for extra respiratory support while you closely watch their trajectory and stay ready to escalate.

References1. RENOVATE Investigators and BRICNet Authors.
High-flow nasal oxygen vs noninvasive ventilation in patients with acute respiratory failure: The RENOVATE randomized clinical trial. JAMA. 2025;333(10):875–890.
PMID: 39657981 2. Tempo G, Grieco DL.
Article review: The RENOVATE randomised clinical trial. European Society of Intensive Care Medicine (ESICM) Article Review. 2025.
Available here 3. Roca O, Messika J, Caralt B, et al.
Predicting success of high-flow nasal cannula in pneumonia patients with hypoxemic respiratory failure: The utility of the ROX index. J Crit Care. 2016;35:200–205.
PMID: 27481760 4. Rochwerg B, Brochard L, Elliott MW, et al.
Official ERS/ATS clinical practice guidelines: Noninvasive ventilation for acute respiratory failure. Eur Respir J. 2017;50(2):1602426.
PMID: 28860265 Post Peer Reviewed By: Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO), Frank Lodeserto, MD and Anand Swaminathan, MD (X: @EMSwami)

Guest ContributorJonathan Bradshaw, DO
Emergency Medicine Resident (PGY-3)
Cape Fear Valley Medical Center
Fayetteville, NC

Your Deep-Dive Starts Here###### REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia)

In this episode, we break down a practical bedside approach to hypoxemia. We ...

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REBEL RundownKey Points Rest isn’t a luxury; it’s a necessity and differs significantly from sleep in terms of mental and physical recovery needs.

Uncovering the seven types of rest can highlight diverse needs: physical, mental, sensory, creative, emotional, social, and spiritual.

Rest from high-stress environments such as the ED is crucial for reducing exhaustion, enhancing decision-making, and maintaining empathy.

The necessity for intentional rest: tailor your rest strategies to meet personal recharge needs effectively.

Rest should be deserved, not earned—it’s a vital component of overall health and wellness, on par with nutrition and hydration.

Click here for Direct Download of the Podcast.

Previously Covered and Related Content: + REBEL Core Cast: Sleep Hygiene + Rebellion in EM: Care For Yourself – Sleep Hygiene + First10EM: Some Evidence For Working Night Shifts + REBEL MIND: Dunning Kruger Effect IntroductionWelcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during D*ifficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine.

Today we are exploring the imperative topic of rest and why it’s not just about sleeping. The first of a two part series, hosted by Dr. Mark Ramzy with guests Dr. Maureen Aiad and Dr. Amil Badoolah, our discussion sheds light on the multifaceted nature of rest, especially in the demanding field of emergency medicine. If you’re a clinician striving to perform at your best under pressure, this episode offers valuable insights into achieving the rest you deserve.

Cognitive QuestionHow do healthcare professionals in high-stress environments distinguish between rest and sleep, and how can they effectively incorporate various types of rest into their routines to manage stress and improve performance?

How is Rest Different From Sleep? + Sleep is biological. It’s essential—but it’s only one form of recovery. + Rest, on the other hand, is intentional, multifaceted, and active. + You can sleep for 8 hours and still feel depleted—because what you needed wasn’t sleep, it was rest—in a different dimension. How This Applies to the Emergency Department or ICU? + In the fast-paced, high-pressure world of the ED or ICU, medical professionals often overlook the importance of rest, perceiving it as unproductive. + Yet, rest is crucial for maintaining cognitive function and emotional resilience. The unique concept of rest outlined in the ‘seven types of rest’ can be particularly beneficial. + Understanding and implementing these can help practitioners handle the rigors of patient care and decision-making more effectively. 7⃣The Seven Types of Rest + 1⃣Physical Rest*: Passive (like sleep) and active (like stretching, massage, gentle movement). + 2⃣*Mental Rest*: Reducing decision fatigue. Tools like brain dumping, meditation, or taking real breaks during work. + 3⃣*Sensory Rest:* This involves reducing the input from your senses, such as limiting screen time, turning off the lights, or enjoying quiet time. + 4⃣*Creative Rest*: Reconnecting with awe. Nature, art, music—things that refill your inspiration tank + 5⃣*Emotional Rest:* Being around people you don’t have to perform for. Saying “I’m not okay.” spaces and people where you can be your authentic self and be at peace + 6⃣*Social Rest*: Taking space from draining interactions; spending time with life-giving people. + 7⃣*Spiritual Rest*: Connection to a greater purpose—faith, community, reflection, meditation Immediate Action Steps for Your Next Shift1. Identify Your Rest Needs: Reflect on what kind of fatigue you’re experiencing and tailor rest activities accordingly, whether it’s sensory detox or emotional unwinding. 2. Practice Sensory Rest: Take brief moments to close your eyes, or step outside for fresh air to manage overstimulation during shifts. 3. Plan Intentional Breaks: Schedule specific times for rest that focus on particular dimensions you identify as lacking. 4. Engage in Active Rest: Incorporate activities like stretching or meditation during your breaks to enhance mental clarity and reduce physical exhaustion. 5. Connect with Supportive Colleagues: Seek interactions with peers who offer emotional and social support, promoting a healthy work-life balance. The Many Aspects of What Makes Up Rest* + Rest is multifaceted – it comes in more than one form + Rest is productive – it improves performance, decision-making, empathy + Rest is intentional – it requires thoughtful engagement, not autopilot. Make a real plan + Rest is layered – especially sensory, which uses all 5 senses + Rest is about input and detox – what you consume, and what you remove. Social rest is a good example + Rest is personal – one person’s recharge is another’s stressor + Rest is deserved, not earned** – full stop. ConclusionRest is a pivotal, multi-dimensional tool that extends beyond mere sleep. For healthcare professionals navigating the strenuous environment of an emergency setting, recognizing and implementing varied forms of rest can enhance overall well-being, decision-making, and patient care. Make rest a deliberate part of your routine, understand its different forms, and remember that it’s a necessity you deserve.

Clinical Bottom LineIncorporating rest into your lifestyle aligns with the demands of your professional roles and personal health needs. By understanding and employing various types of rest, you not only support your individual wellness but also enhance your ability to care for patients effectively. Rest is vital; it is not a privilege earned but an essential right you deserve every day.

Further Reading1. Dalton-Smith, S.
Sacred Rest: Recover Your Life, Renew Your Energy, Restore Your Sanity. Hachette Nashville, 2017. 2. Dalton-Smith, S.
The 7 Types of Rest: Seven Ways to Live a More Energized Life. Hachette Book Group, 2022 3. Abramson, A
“Seven types of rest to help restore your body’s energy.” American Psychological Association, 6 May 2025,
Link is Here Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ * * Maureen Aiad, DOAssistant Professor of Emergency MedicineNYU Grossman Long Island School of Medicine, New York * Amil Badoolah, DOAssistant Professor of Emergency MedicineNYU Grossman Long Island School of Medicine, New YorkShowing Slide 1 of 3###### REBEL Core Cast 119.0 – Sleep Hygiene

REBEL Core Cast 119.0 – Sleep Hygiene Click here for Direct Download of ...

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REBEL Rundown Key Points Hydrocortisone Saves Lives:
The 2023 Cape Cod Trial (NEJM) showed a clear mortality benefit and reduced need for intubation in severe CAP patients treated with hydrocortisone. * Guidelines Are Catching Up:
The SCCM (2024) and ERS now recommend steroids for severe CAP, while ATS/IDSA updates are still pending. * Redefining “Severe”:
Patients requiring high FiO₂ (>50%), noninvasive or mechanical ventilation, or PSI >130 meet criteria for steroid therapy — even outside the ICU. * Main Risk = Hyperglycemia:
Elevated glucose was the most consistent adverse effect, but rates of GI bleed and secondary infection were not increased. * Early, Targeted Use Matters:
Start hydrocortisone within 24 hours* of identifying severity — especially in patients with high CRP (>150) or strong inflammatory response. Click here for Direct Download of the Podcast.

IntroductionCorticosteroids have long sparked debate in the treatment of bacterial pneumonia — once viewed with skepticism, now increasingly supported by high-quality evidence. In this episode, Dr. Alex Chapa joins the REBEL Core Cast team to explore how the 2023 Cape Cod Trial (NEJM) reshaped practice and guideline recommendations for severe community-acquired pneumonia (CAP).

Historical Context & Long-Standing SkepticismFor decades, the use of steroids in pneumonia was controversial.

• • Early Use: Steroids entered practice in the 1940s and 50s for autoimmune inflammation, but there was immediate hesitation regarding secondary superinfections.
  • Mixed Data: From the 1980s to the 2000s, small studies emerged on severe pneumonia and ARDS, but the data was inconsistent. Different trials used varying definitions of “severe” pneumonia and different C-reactive protein (CRP) cutoffs, making the data “spread” and easy to “cherry pick” to support or deny a benefit.
  • Past Guidelines: This uncertainty was reflected in official guidelines:
    • 2007 (ATS/IDSA): The American Thoracic Society and the Infectious Diseases Society of America did not address the topic due to insufficient data.
    • 2019 (ATS/IDSA): Pre-COVID, the guidelines recommended against using corticosteroids in severe CAP. They acknowledged no benefit for non-severe pneumonia, but the data for severe pneumonia was considered too weak to endorse.
    • Pre-Trial Consensus: Prior to 2023, the consensus was to avoid steroids in non-severe pneumonia, while severe pneumonia remained a “gray area” with no treatment showing a clear mortality difference. The Landmark Cape Cod Trial (NEJM 2023)The Cape Cod trial, published in the New England Journal of Medicine in 2023, reignited the discussion by providing robust, positive data.

• Trial Design: Phase 3, multi-center, double-blind, randomized, controlled trial.

• Intervention: 800 patients randomized to two groups, Hydrocortisone as a continuous infusion (200mg/day) versus a placebo infusion.
• Taper: On day 4, clinicians would decide whether to continue the infusion or begin a taper based on clinical response.
• Population: Patients with severe CAP, defined by meeting at least one of the following criteria:
  • Pneumonia Severity Index (PSI) > 130.
  • O2 by FiO2 ratio < 300.
  • Need for mechanical or non-invasive ventilation (with PEEP ≥ 5).
  • Need for high FiO2 (>50%) via non-rebreather or heated high flow.
• Primary Outcomes: Death for any cause 6.2% (hydrocortisone) vs 11.9% (placebo)
• Secondary outcomes:
  • Death from any cause at 90 days 9.3% (hydrocortisone) vs 14.7% (placebo)
  • Endotracheal intubation 18% (hydrocortisone) vs 29% (placebo)
  • Hospital-acquired infections 9.8% (hydrocortisone) vs 11.1% (placebo)
  • Gastrointestinal bleeding 2.3% (hydrocortisone) vs 3.3% (placebo)
  • Vasopressor initiation by day 28 15.3% (hydrocortisone) vs 25.0% (placebo)

• Key Findings: The trial demonstrated superiority for hydrocortisone Updated Guidelines & Current PracticeThe Cape Cod trial, along with subsequent meta-analyses, has begun to change official recommendations.

• Society of Critical Care Medicine (SCCM): In 2024, an SCCM expert panel, reviewing the Cape Cod trial and 18 others, strongly recommended corticosteroids for severe CAP. They concluded that steroids reduce mortality and the need for mechanical ventilation.

• Meta-Analysis (Smit et al.): A 2024 meta-analysis in Lancet Respiratory confirmed the 30-day mortality benefit.
• European Respiratory Society (ERS): The ERS has issued a recommendation to use steroids for severe pneumonia but still urges caution regarding side effects.

• ATS/IDSA: As of the podcast recording, the ATS/IDSA had not yet updated their 2019 guidelines. Practical Application for CliniciansDefining “Severe” CAP: The key is to identify patients who qualify as “severe”. This can be done using:

• Scoring Tools: The PSI is the best validated tool for mortality but is cumbersome. Simpler tools like CURB-65 or SMART-COP are practical and acceptable for defining severity. 2023 meta-analysis from by Zaki et al showed both work well, but CURB-65 has better mortality prediction early on.

• Cape Cod Criteria: Any patient meeting the trial’s inclusion criteria (e.g., high-flow O2, non-invasive ventilation) qualifies, regardless of location (ED, floor, or ICU).
• Biomarkers: While not required, a CRP level was used in many studies. A CRP > 150 (Cape Cod) or > 204 (Smit meta-analysis) strongly indicates severe inflammation that would benefit from steroids.
• Clinical Judgment: A patient who looks “sick,” has “soft” blood pressure, or has dense infiltrates and high oxygen needs (e.g., >50% FiO2 on high flow) is a candidate.

Adverse Effects:

• Hyperglycemia: This was the most significant risk identified, with rates between 6-12%. This is a primary concern, especially in patient populations with high BMI.
• GI Bleed & Secondary Infection: Fears of these side effects, which contributed to historical skepticism, were not borne out in the Cape Cod trial. The data does not support being overly concerned.

• Other Side Effects: Mood changes, delirium, insomnia, and agitation in the elderly are known side effects of steroids that were not specifically addressed in the trial but remain clinical concerns. Clinical Pathway for Steroids in Severe CAPUnanswered Questions & Future ResearchPossible remaining questions:

• Biomarkers: Can we find a more precise CRP level to distinguish moderate from severe disease? Could other markers like ferritin or IL-6 be used?

• Dosing & Tapering: How much immunomodulation is needed, and when is it truly safe to taper?
• Gender Differences: Early data suggests females may respond better to steroids and experience fewer side effects. The question of female patients with severe CAP require less corticosteroids needs further exploration. Clinical Bottom LineThe current literature, spearheaded by the Cape Cod trial, now supports the use of corticosteroids in severe community-acquired pneumonia. The best evidence currently points to hydrocortisone, started early (within 24 hours) after severity is identified using a validated tool. While hyperglycemia is a risk, the previous fears of GI bleeding and secondary infections were not substantiated in recent, rigorous trials.

References1. Chapa-Rodriguez A, Abou-Elmagd T, O’Rear C, Narechania S.
Do patients with severe community-acquired bacterial pneumonia benefit from systemic corticosteroids?. Cleve Clin J Med. 2025;92(10):600-604.
PMID: 41033846 2. Dequin PF, Meziani F, Quenot JP, et al.
Hydrocortisone in Severe Community-Acquired Pneumonia. N Engl J Med. 2023;388(21):1931-1941.
PMID: 36942789 3. Chaudhuri D, Nei AM, Rochwerg B, et al.
2024 Focused Update: Guidelines on Use of Corticosteroids in Sepsis, Acute Respiratory Distress Syndrome, and Community-Acquired Pneumonia. Crit Care Med. 2024;52(5):e219-e233.
PMID: 38240492 Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Show Notes Alex Chapa, MDPGY 5 Pulmonary Critical Care FellowCape Fear Valley Medical CenterFayetteville NCShowing Slide 1 of 1 Your Deep-Dive Starts Here###### REBEL Core Cast 149: Review of Corticosteroids in Community-Acquired Pneumonia

Corticosteroids have long sparked debate in the treatment of bacterial ...

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REBEL RundownIntroductionWelcome to this special edition of the REBEL Cast, where we unravel key highlights and educational insights from the IncrEMentuM Conference in Spain. This event is a cornerstone for advancing emergency medicine education, drawing esteemed speakers and participants from around the globe. As emergency medicine gains traction in Spain, this conference has become an essential platform for knowledge exchange and professional growth. Today, host Dr. Mark Ramzy shines a spotlight on two phenomenal educators: Drs. Sara Crager and Ryan Ernst who shared their expertise and experiences at this transformative gathering last spring.

Click here for Direct Download of the Podcast.

What's IncrEMentuM?A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals.

What's an Essential Question?Essential questions are open-ended, thought-provoking, and intellectually engaging inquiries that inspire deeper exploration into topics. In the context of medical education, they challenge practitioners to think critically and reflect on their practice deeply. By focusing on essential questions, medical educators aim to inculcate a culture of continuous learning and curiosity, ensuring that medical professionals stay adaptable and insightful in their approach to patient care.

Rapid Sequence (no not the intubating style...)The Rapid Sequence game is an innovative tool that Sara and Ryan designed to enhance the learning experience for emergency medicine clinicians. It mimics real-life scenarios requiring rapid decision-making in high-pressure situations, such as those faced in emergency medical settings. This clinical case-based game aims to improve cognitive and procedural skills, allowing participants to hone their ability to respond effectively under pressure, thereby enhancing their real-world clinical performance.

You can try it out for free on their website here!

Their work was featured in the September 2025 edition of Annals of Emergency Medicine as a 2025 ACEP Abstract

The Arboretum Teaching CollectiveAn arboretum is a space that cultivates a wide variety of diverse, unique, and symbiotic growth. Arboretum provides a creative space to decrease barriers, open opportunities, and support the development of extraordinary teachers. The Arboretum Teaching Collective is a non-profit organization dedicated to supporting emergency medicine education in countries where it is a new or evolving specialty. Their aim to facilitate the development of expert teachers by reducing barriers, providing opportunities, and curating talent. Their goal is to create a community of educators around the globe who share a vision of bringing excellent, innovative emergency medicine teaching to where it is most needed. Their approach is driven by curiosity, humility, and sustainability.

If you want to learn more and get involved, check out the Arboretum Teaching Collective Website Here

See you in Spain!The upcoming conference aims to gather world-class educators once more and promises an enriching experience for all attendees. Drs. Sara Crager and Ryan Ernst, along with many others, will be there at the event. For more information on the IncrEMentuM Conference and to register, visit their website! See you there!

Sara Crager, MDAssociate Professor, Critical Care and Emergency MedicineUCLA, Los Angeles, CA * * * Ryan Ernst, MDAssistant Professor of Emergency Medicine, Section Chief of Global EMUniversity of Utah, Salt Lake City, UT Mark Ramzy, DOCo-Editor-in-ChiefRutgers Health / RWJBH, Newark, NJ* * * Showing Slide 1 of 3 Your Deep-Dive Starts Here###### REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Sara Crager and Ryan Ernst

Host Dr. Mark Ramzy shines a spotlight on two phenomenal ...

ResuscitationRead More###### REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Tarlan Hedayati, Jess Mason and Simon Carley

Host Dr. Mark Ramzy shines a spotlight on three distinguished ...

ResuscitationRead More###### REBEL CAST – IncrEMentuM26 Speaker Spotlight : George Willis and Mark Ramzy

REBEL Rundown Introduction In this exciting episode of REBEL ...

Endocrine, Metabolic, Fluid, and ElectrolytesRead More###### Incrementum Conference 2026: Revolutionizing Emergency Medicine in Spain

In this special episode of Rebel Cast, we spotlight the ...

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REBEL Rundown Key Points Building Resilience: Rebel MIND, in partnership with Arena Labs, introduces a science-based performance coaching platform specifically tailored for healthcare professionals, focusing on stress management and burnout prevention.
Personal Insights: Jackie Penn shares her journey from exercise science to digital coaching, highlighting the importance of tailored coaching in high-pressure environments like healthcare.
Clinician-Centric Approach: Understanding unique challenges faced by ER doctors, the program provides practical tools for stress and transition management, improving both professional and personal life balance.
Revolutionary Wearables: Utilizing wearables, the program offers objective feedback on recovery and health metrics, allowing personalization of strategies to enhance clinician well-being.

Click here for Direct Download of the Podcast.

IntroductionWelcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, we’re excited to continue collaboration with Arena Labs, where host Dr. Marco Propersi interviews Jackie Pen, Heading of Performance Coaching at Arena Labs. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.

Previously Covered on REBEL MIND: Performance Under Pressure – What Medicine Can Learn from Elite Teams Cognitive QuestionHow do specific performance coaching strategies and tools assist healthcare professionals, particularly those in emergency medicine, in managing stress and preventing burnout effectively?*

Why This is Important + Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals. How This Applies to the Emergency Department or ICU? + In the chaotic and high-stakes environment of the ED/ICU, healthcare professionals are often required to make split-second decisions under pressure while managing emotional stress. This necessitates not just clinical acumen but also strong emotional resilience and stress management skills. Performance coaching provides the tools and frameworks to enhance these skills, offering strategies like the de-stress breath and transition protocols to help clinicians navigate between high-pressure situations efficiently. These tools are designed to not only improve their professional performance but also ensure they are emotionally present for their personal lives, ensuring a healthier work-life balance. Things You Can Do on Your Next Shift* + Practice the De-stress Breath: Before moving from one critical case to another, take a moment to take two inhales through the nose followed by an extended exhale, helping to reset your nervous system by activating your parasympathetic nervous system. + Implement a Transition Protocol: Choose a point in your journey home to mentally switch from clinician to family member, helping you to be more present outside of work. + Optimize Your Nutrition and Rest: Even small changes during your shift, like meals that promote easy digestion or quick physical activities, can make a significant difference in your energy levels. + Engage with Wearables: If possible, use wearables to monitor your physiological responses, helping tailor personalized strategies for your shifts Where to Learn MoreIntrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance.

Clinical Bottom LineIn an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine.

Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for.

Meet the Authors Marco PropersiCo-Editor-in-ChiefVassar Brothers Medical Center, Poughkeepsie, NY* * Jackie PenHead of Performance CoachingArena LabsShowing Slide 1 of 2The post REBEL MIND: The Power of Performance Coaching in Medicine appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key PointsPartnership Focus: New collaboration with Arena Labs aimed at enhancing healthcare worker wellness.

Personalized Coaching: Tools and coaching programs designed for stress management and performance improvement.

Data-Driven Insights: Utilizing wearable sensor data to tackle burnout effectively.

Broad Impact: Offers a unique opportunity to contribute to large-scale healthcare improvements.

Click here for Direct Download of the Podcast.

IntroductionWelcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, hosted by Drs. Mark Ramzy and Marco Propersi, we’re excited to introduce a collaboration with Arena Labs. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.

Cognitive QuestionWhat would it look like in emergency medicine and critical care to be set up with the same tools as elite teams and professional athletes when it comes to measuring performance and recovery? How would our patients benefit?

Why This is Important + Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals. Be Brilliant at the Basics + Ask yourself — “What is it on your time off that gives you a deep sense of fulfillment?” + On your time off are you doing things that fill your bucket and add to your recovery? What is Allostasis and Allostatic Load + Allostasis: Our body’s ability to adapt over time to stress. It’s relevant to the phase you are in during this particular season in your life. - Ex. You are a first year medical student freaking out about your very first exam. Over time as you do more exams, they are still stressful, but by now you have developed modified study habits to succeed and get used to the frequent exams - In the context of emergency medicine, you may be nervous or stressed about your first shift at a new hospital but overtime you learn the staff, the location of equipment, the acuity of that particular site, the patient population so over time you get used to the stress of a shift at that new hospital * + Allostatic Load*: The wear and tear on the body from chronic stress due to maladaptation or poor recovery methods. * + This refers to the cumulative burden of chronic stress and life events. It involves the interaction of different physiological systems at varying degrees of activity. - Ex. You are an emergency medicine physician at a very busy, high acuity center and have never prioritized taking care of yourself on/during a shift. As a result, external factors add to not being able to fully recover when you get home or are off shift (ie. Admin work, teaching obligations, family/friends) and so you never fully recover before you have to go back on shift to the same stressors you just exposed yourself to. So the cycle continues

Figure 1: Long term effects of Chronic Stress (Source: Andrew Hogue from NeuroFit)

How This Applies to the Emergency Department or ICU?* + Healthcare workers in emergency departments (ED) and intensive care units (ICU) are often under enormous stress due to the nature of their work. Arena Labs’ program offers tailored solutions, helping ED and ICU staff manage their unique challenges through effective recovery techniques and performance tools. This approach caters specifically to the demanding schedules and the unpredictability inherent in these environments. Where to Learn MoreIntrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance.

Clinical Bottom LineIn an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine.

Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for.

References1. Guidi J, et al.
Allostatic Load and Its Impact on Health: A Systematic Review. Psychother Psychosom. 2021; Epub 2020 Aug 14.
PMID: 32799204 2. Frueh BC, et al.
“Operator syndrome”: A unique constellation of medical and behavioral health-care needs of military special operation forces. Int J Psychiatry Med. Epub 2020 Feb 13.
PMID: 32052666 Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ * * Marco PropersiCo-Editor-in-ChiefChair of Emergency Medicine at Vassar Brothers Medical Center, Poughkeepsie, NY * Brain FergusonFounder and CEOArena LabsShowing Slide 1 of 3The post REBEL MIND: Performance Under Pressure – What Medicine Can Learn from Elite Teams appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points NIV = Support without a tube: CPAP, BiPAP, and HFNC improve oxygenation and reduce the work of breathing. * CPAP = Continuous pressure: Best for hypoxemic patients (e.g., pulmonary edema, OSA). * BiPAP = Two pressures (IPAP/EPAP): Great for hypercapnic failure (e.g., COPD, obesity hypoventilation). * HFNC = Heated, humidified high flow: Reduces effort, improves comfort, and enhances oxygen delivery. * Supportive, not definitive:* NIV stabilizes patients while the underlying cause is treated. Click here for Direct Download of the Podcast.

IntroductionNon-invasive ventilation (NIV) refers to respiratory support provided without endotracheal intubation. The most common modalities include continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), and high-flow nasal cannula (HFNC). These therapies aim to improve oxygenation, reduce the work of breathing, and potentially prevent invasive mechanical ventilation.

CPAP and BiPAP CPAP delivers a single, continuous pressure during inspiration and expiration. This pressure (commonly 5–10 cm H₂O) helps recruit atelectatic alveoli, reduce shunt, and improve oxygenation. It is commonly used for conditions like pulmonary edema, obstructive sleep apnea, or mild hypoxemia without significant ventilatory failure. * BiPAP alternates between two pressures: + Inspiratory positive airway pressure (IPAP), augments tidal volume and unloads inspiratory muscles. + Expiratory positive airway pressure (EPAP), maintains alveolar recruitment and improves oxygenation.
The differential between IPAP and EPAP is critical for reducing hypercapnia in patients with COPD exacerbations or acute hypercapnic respiratory failure. * Indications + CPAP: hypoxemia without major ventilatory failure (e.g., cardiogenic pulmonary edema, atelectasis, OSA). + BiPAP: hypercapnia with increased work of breathing (e.g., COPD exacerbation, neuromuscular weakness, obesity hypoventilation). * A helpful way to conceptualize CPAP and BiPAP is through the hairdryer analogy. Imagine placing a hairdryer in your mouth: Clinical Considerations Masks can be uncomfortable, impair secretion clearance, and limit oral intake. * Some patients require sedation to tolerate NIV, but this carries risks in patients with unprotected airways. * NIV is thus a high-stakes intervention requiring close monitoring. * Common starting dose to understand titration, but start at the level appropriate for your patient: IPAP 10 cm H₂O / EPAP 5 cm H₂O (“10/5”) and are titrated: + Increase IPAP to improve tidal volume and CO₂ clearance. + Increase EPAP to recruit alveoli and improve oxygenation. + Both may be raised simultaneously if the patient is both hypoxemic and hypercapnic. High-Flow Nasal Cannula (HFNC) H: Heated & humidified – improves mucociliary clearance, prevents airway drying, and enhances tolerance. I: Inspiratory flow – high flow meets or exceeds patient demand, reducing respiratory rate and effort. * F: Functional residual capacity – modest generation of positive end-expiratory pressure (PEEP), promoting alveolar recruitment. * L: Lighter – generally more comfortable and less restrictive than mask-based NIV. * O: Oxygen dilution – minimizes entrainment of room air, delivering higher and more predictable FiO₂. * W: Washout – flushes anatomical dead space, reducing CO₂ rebreathing. * HFNC delivers heated, humidified oxygen at high flow rates (30–60 L/min) through wide-bore nasal prongs. A mnemonic, H-I-F-L-O-W, helps summarize its mechanisms: * Indications: Traditionally used for acute hypoxemic respiratory failure (e.g., pneumonia), HFNC is increasingly studied for hypercapnic failure as well, with trials suggesting non-inferiority to BiPAP in select populations. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)*

Show Notes Syed Moosi Raza, MDPGY 3 Internal Medicine ResidentCape Fear Valley Internal Medicine Residency ProgramFayetteville NCAspiring Pulmonary Critical Care FellowShowing Slide 1 of 1 Your Deep-Dive Starts Here###### REBEL Core Cast 1.0 – The Intro

REBEL EM-ers: Salim, Jenny and I would like to announce ...

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REBEL Rundown Key Points Mortality: No statistically significant difference in 28-day mortality between ketamine vs etomidate for intubation in critically ill patients, though there was a ~1% absolute difference favoring ketamine. * Hemodynamics: Ketamine induction was associated with more cardiovascular collapse, mainly driven by new/increased vasopressor use* (dose escalation or addition of a vasoactive agent). Click here for Direct Download of the Podcast.

IntroductionEtomidate or ketamine? The debate over the ideal agent for emergency rapid sequence intubation (RSI) has raged for years with no clear winner. Etomidate has been touted in the past for its rapid onset and minimal intrinsic effects on hemodynamics. However, the drug is well known as a transient adrenal suppressant though the impact of this suppression isn’t clear. Ketamine has risen in recent years as an alternative, due to its perceived hemodynamic stability, analgesic properties and absence of adrenal suppression. Additionally, recent data points towards improved mortality when ketamine was selected over etomidate (Kotani 2023). High quality randomized controlled trials are needed to further elucidate which agent should be selected in critically ill patients.

PaperCasey JD et al. Ketamine or etomidate for tracheal intubation of critically ill adults. NEJM 2025. PMID: 41369227

Previously Covered On REBEL REBEL EM: The EvK Trial: Ketamine vs Etomidate for Rapid Sequence Intubation * REBEL EM: From Debate to Data: Emerging Insights into RSI Induction with Ketamine vs Etomidate* What They DidCLINICAL QUESTIONIn critically ill adults undergoing tracheal intubation, does the use of ketamine instead of etomidate result in improved 28 day mortality?

STUDY DESIGNMulticenter, randomized, open-label trial in both emergency departments and ICUs.

POPULATION

| Inclusion Criteria: Critically ill patients > 18 years of age undergoing tracheal intubation with the use of an induction agent | Exclusion Criteria: Known pregnancy * Prisoners * Primary diagnosis of trauma * Need for immediate intubation precluding randomization * Clinicians determined that the use of ketamine or etomidate was either necessary or contraindicated |

INTERVENTION & COMPARATOR

| Ketamine Arm: Ketamine administered based on a provided nomogram: full dose (2.0 mg/kg), intermediate dose (1.5 mg/kg) or reduced dose (1.0 mg/kg) | Etomidate Arm:** Etomidate administered based on a provided nomogram: full dose (0.3 mg/kg), intermediate dose (0.25 mg/kg) or reduced dose (0.2 mg/kg) |

OUTCOMES Primary: In-hospital death from any cause by day 28. * Secondary: * + - Cardiovascular collapse during intubation defined as SBP < 65 mm Hg, receipt of new or increased dose of vasopressors or cardiac arrest. * Exploratory Procedural: * + - Lowest systolic blood pressure - Lowest systolic blood pressure below 80 mmHg - Highest systolic blood pressure above 180 mmHg - Lowest oxygen saturation - Lowest oxygen saturation below 80% - Successful first attempt intubation - Time from induction to intubation * Exploratory Clinical: * + - Number of ventilator free days - Vasopressor-free days - ICU free days * Safety: * + Systolic blood pressure at 24 hours after enrollment + Ongoing receipt of vasopressors at 24 hours Results: 2365 patients were randomized + Ketamine: 1176 + Etomidate: 1189 * > 99% of patients received the drug they were randomized to receive * NMBA: 69% of patients in both groups received rocuronium * ~ 95% of patients had video laryngoscopy for the primary intubation attempt Critical Results Strengths Multicenter ED + ICU cohort of critically ill patients → improves external validity * Strong randomization → balanced baseline characteristics * Right population for the question → appropriately focused on a sick cohort where induction choice matters most * High protocol adherence → most patients received the agent they were randomized to * Excellent follow-up → minimal loss to follow-up / outcome capture Limitations No blinding → potential performance/resuscitation bias * Trauma excluded → limits applicability to peri-intubation trauma care * Case-mix skewed toward septic shock → may reduce generalizability to other shock etiologies * Power assumptions → designed to detect a 5% mortality difference (possibly overly ambitious) * Equipoise-only enrollment → excluded patients with clear indication/contraindication → selection bias + reduced real-world applicability * Composite secondary outcome with non-equivalent endpoints (e.g., cardiac arrest vs vasopressor titration) * Ketamine dosing by actual body weight (vs ideal) → may have increased dose/exposure in some patients Discussion The increase in cardiovascular collapse seen with ketamine was driven by the “new or increased vasopressor use” piece of the composite outcome not by the more clinically relevant severe hypotension (SBP < 65 mm Hg) or cardiac arrest. * The increase in CV collapse is a secondary outcome and hypothesis generating only * Care beyond induction agent isn’t clearly delineated and may have varied between groups * Reasons why there was more CV collapse in the ketamine group: + Patients in the etomidate group were more likely to be on pressors or have pressor increases prior to induction agent administration + Ketamine has analgesic properties which may affect hemodynamics (etomidate does not have analgesic effects) + The standard ketamine dose of 2 mg/kg is higher than the induction dose used by most (1-1.5 mg/kg) + Ketamine dosing was based on actual body weight though ideal body weight dosing is more accepted. This may have resulted in unnecessarily large ketamine doses that may have had a greater effect on hemodynamics. * This is a study of patients with clinical equipoise + Patients who the clinician determined would clearly benefit from one agent or the other or in whom one agent or the other was contraindicated were excluded from the study. + This may add a selection bias to the results. * Clinicians were not blinded to the induction agent administered + The absence of blinding can introduce bias. + For instance, knowledge of the agent the patient was randomized to may result in different resuscitative treatment prior to intubation. * An induction agent nomorgram was provided to allow clinicians to choose their induction dose depending on patient stability. * A 5% difference in mortality may be overly ambitious. As Josh Farkas points out in his post on this article, PCI for STEMI only has a 3% absolute difference in mortality versus standard care. * The 1% absolute difference in mortality while not statistically significant would be clinically significant if it was real. + The study would have to be much larger to show a statistically significant 1% difference. * About 2% of patients in each group received additional medications during induction (propofol, benzodiazepines, opiates). It is unclear why these agents were selected in specific cases and how they may have affected the outcomes in question. Author's Conclusion“Among critically ill adults undergoing tracheal intubation, the use of ketamine to induce anesthesia did not result in a significantly lower incidence of in-hospital death by day 28 than etomidate.*“

Our ConclusionIn this well done RCT, induction with ketamine did not result in a lower 28-day mortality when compared to induction with etomidate in critically ill adults. The secondary outcome of an increase in cardiovascular collapse is interesting and should be studied more in the future.

Clinical Bottom LineThis data should not drive clinicians to abandon the use of ketamine in RSI. To the contrary, the study leaves open the possibility of a clinically meaningful difference in mortality favoring ketamine that may be borne out in a larger study. However, etomidate can be considered as a first-line option for RSI and may be the superior drug in patients at high-risk for cardiovascular decompensation.

Post Peer Reviewed By: Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO) and Marco Propersi, DO

ReferencesKotani Y et al. Etomidate as an induction agent for endotracheal intubation in critically ill patients: a meta-analysis of randomized trials J Crit Care 2023;77:154317. PMID: 37127020

Associate Author###### Anand Swaminathan

MD, MPHAll Things REBEL EM

Meet The Team Your Deep-Dive Starts Here###### The RSI Trial: Ketamine vs Etomidate in Rapid Sequence Intubation

Etomidate or ketamine? The debate over the ideal agent for emergency rapid sequence ...

ResuscitationRead More###### REBEL Cast Ep120: Etomidate vs Ketamine for RSI in the ED?

Background: Standard rapid sequence intubation (RSI) in the emergency department involves administration of ...

Procedures and SkillsRead MoreShowing Slide 1 of 3The post The RSI Trial: Ketamine vs Etomidate in Rapid Sequence Intubation appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points We don’t know what we don’t know: Low experience can inflate confidence; true expertise usually brings humble certainty.

ED relevance is universal: From central lines to transvenous pacing, over- or under-confidence shows up at every level—intern to seasoned attending.

Metacognition matters: Accurate self-assessment is a clinical skill; reflection + feedback loops keep us calibrated.

Practice beats bravado: Skill decay is real; deliberate practice and HALO (high-acuity, low-occurrence) refreshers protect patients.

Psychological safety ≠ niceties: “Confident humility” enables questions, feedback, and better resuscitation decisions—especially under uncertainty.

Click here for Direct Download of the Podcast.

IntroductionWelcome to REBEL MIND—Mastering Internal Negativity during Difficulty. In this series, we turn the same critical lens REBEL EM uses for literature inward—into mindset, leadership, and psychological safety—so we can deliver better care outward to patients and teams.

In this episode and blog post, hosts Mark Ramzy and Kim Bambach (Assistant Professor of Emergency Medicine, The Ohio State University) explore a deceptively simple question: How accurately can we assess our own performance? The answer hinges on a classic cognitive bias that touches all of us in emergency medicine.

PaperKruger J, Dunning D. Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments. J Pers Soc Psychol. 1999 Dec;7 PMID: 10626367

Cognitive QuestionHow accurately can we assess our own performance?

What is the Dunning-Kruger Effect?The Dunning–Kruger Effect is a cognitive bias where:

• Lower-skill individuals tend to overestimate their competence, and
• Higher-skill individuals often underestimate theirs.

Translation for the busy clinician: early on the learning curve, confidence spikes (“Mount Stupid”) because we don’t yet see the complexity. As experience accrues, confidence dips (“Valley of Despair”) with growing awareness, then rises again—grounded in nuance and humility.
Key insight: True expertise ≠ louder certainty; it’s often quieter, more curious, and more collaborative.

How It Applies to the Emergency Department Procedures (e.g., central lines, TVP): Watching a 5-minute video creates “I got this” energy—until the wire won’t pass, the patient thrashes, or you hit carotid. Competence includes troubleshooting in context. * Skill Decay is Inevitable: If you haven’t done a chest tube or a TVP in months, you’re not as sharp as last time. Without deliberate refreshers, you drift below the safe-performance line. * Everyone’s a Novice Somewhere: New disease entities, evolving algorithms, new tools (POCUS, decision support) mean even attendings routinely re-enter novice zones. * Feedback Blind Spots: Lower performers can both overestimate their skills and resist feedback—while many high performers (particularly women, per discussed literature) undervalue their abilities. * Culture is Clinical: The ED demands decisive action amid uncertainty. Psychological safety + confident humility lets teams surface alternative diagnoses, challenge momentum, and correct course fast. Immediate Action Steps for Your Next Shift1. Run a 60-second debrief on two casesWhat went well? What would I do differently next time?
Write one improvement you’ll test today. 2. Play “What if the opposite were true?”Anchored on “lumbosacral strain”, Ask, What if fever/incontinence appears? How does that change my path? 3. Solicit 360° micro-feedbackAsk a nurse, resident, and peer: “One thing I did well; one thing to improve.” Say “thank you,” not “but.” 4. Schedule a HALO refresher this weekPick one high-acuity, low-occurrence procedure (TVP, cric, thoracotomy).
Do a 10-minute mental model + equipment walk-through; book sim time if available. 5. **Adopt a pre-procedure pauseIf X goes wrong, I’ll do Y.
Name two likely failure modes (e.g., “wire won’t advance,” “delirium/agitation”) and your first corrective step. 6. Language shift on shiftSwap “I’m sure” → “I’m reasonably confident, here’s my plan B.” Invite input: “What am I missing?” ConclusionThe Dunning–Kruger Effect isn’t a moral failing; it’s a predictable human pattern that every clinician rides—often multiple times per day in the ED. The antidote is metacognition*: routine reflection, explicit debiasing, deliberate practice, and feedback within a psychologically safe culture.

Clinical Bottom LineCompetence is quiet and curious. The more we know, the more we recognize what we don’t—and the better we become at caring for patients and each other.

Further Reading1. Dunning D, Kruger J. Unskilled and Unaware of It (1999). Classic paper introducing the effect. 2. Croskerry P. Cognitive forcing strategies in clinical decision-making. 3. Kahneman D. Thinking, Fast and Slow. Heuristics & biases in high-stakes decisions. 4. Ericsson KA. Peak: Secrets from the New Science of Expertise. Deliberate practice & skill acquisition. 5. Edmondson AC. The Fearless Organization. Psychological safety and learning culture in teams. Meet the Authors Mark Ramzy, DOCo-Editor-in-ChiefCardiothoracic Intensivist and EM AttendingRWJBH / Rutgers Health, Newark, NJ* * * Kim Bambach, MDPodcasting ManagerAssistant Professor of Emergency MedicineOhio State UniversityShowing Slide 1 of 2The post REBEL MIND – The Dunning Kruger Effect: Why Looking Inward Improves Patient Care appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points Peak vs. Plateau Pressures: PIP reflects total airway resistance and compliance, while Pplat isolates alveolar compliance—elevations in both suggest decreased lung compliance (e.g., ARDS, pulmonary edema, pneumothorax). * PEEP Protects Alveoli: Maintains alveolar recruitment and prevents collapse; typical range 5–8 cmH₂O, but higher levels may benefit moderate–severe ARDS. * Driving Pressure (ΔP = Pplat − PEEP): Lower ΔP reduces atelectrauma and improves outcomes; optimize by adjusting PEEP thoughtfully. * Prevent VILI: Keep Pplat < 30 cmH₂O, use low tidal volumes (6 mL/kg IBW), and monitor for barotrauma, volutrauma, atelectrauma, and biotrauma. * Evidence-Based Practice:* ARDSNet and subsequent trials confirm that lung-protective ventilation—low Vt, limited pressures, and individualized PEEP—improves survival in ARDS. Click here for Direct Download of the Podcast.

IntroductionThis episode reviews essential ventilator pressures and how to interpret them during ICU rounds.

Under Pressure1. Peak Inspiratory Pressure (PIP) * Definition: Total pressure required to deliver a breath. * Reflects: Airway resistance + lung/chest wall compliance. * Common Causes of ↑ PIP: + Mucus plugging + Biting the endotracheal tube + Kinked tubing or bronchospasm 2. Plateau Pressure (Pplat) * Definition: Alveolar pressure measured after an inspiratory hold. * Reflects: Lung compliance (stiffness of lung tissue). * When Both PIP & Pplat Are Elevated:
→ Indicates poor compliance (e.g., ARDS, pulmonary edema, pneumothorax). 3. Positive End-Expiratory Pressure (PEEP) * Definition: Pressure remaining in airways at end-expiration to prevent alveolar collapse. * Typical Range: 5–8 cmH₂O but needs to titrated to meet patient requirements * Notes: + Provides physiologic “glottic” PEEP in intubated patients. + Using high PEEP strategy shows mortality benefit only in moderate–severe ARDS in meta-analysis. 4. Driving Pressure (ΔP) * Definition: ΔP = Pplat − PEEP. * Reflects: Pressure needed to keep alveoli open during the respiratory cycle. * Goal: Lower ΔP → less atelectrauma & improved outcomes. * Optimize: Increase PEEP to reduce ΔP and alveolar cycling. Interpreting High PIP/High Pplat ↑ PIP & ↑ Pplat + Interpretation: ↓ Compliance + Common Causes: ARDS, pulmonary edema, pleural effusion, pneumothorax * ↑ PIP & Normal/Low Pplat + Interpretation: ↑ Airway Resistance + Common Causes: Mucus plug, bronchospasm, tube obstruction or biting Ventilator-Associated Lung Injury (VILI)1. Barotrauma: * Mechanism: Excessive airway pressure damages alveoli. * Prevention: Keep Pplat < 30 cmH₂O. 2. Volutrauma: * Mechanism: Overdistension from excessive tidal volumes. * Prevention: Use low tidal volume ventilation (6 mL/kg ideal body weight). * ARDSNet trial: 6 mL/kg → lower mortality compared to 12 mL/kg. * Ideal Body Weight: Based on height and sex, not actual weight. * Typical patient: Tidal Volume: 6–8 mL/kg IBW * ARDS: Tidal Volume: 4–6 mL/kg IBW 3. Atelectrauma: * Mechanism: Repeated opening/collapse of unstable alveoli. * Prevention: Optimize PEEP to keep alveoli open and reduce driving pressure. 4. Biotrauma: * Mechanism: Inflammatory cascade (↑ IL-6, TNF-α) from mechanical injury. * Effect: Can trigger systemic inflammation & multiorgan dysfunction. * Prevention: Minimize all other forms of VILI. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)*

Show Notes Joel Rios Rodriguez, MDPGY 3 Internal Medicine ResidentCape Fear Valley Internal Medicine Residency ProgramFayetteville NCAspiring Pulmonary Critical Care FellowShowing Slide 1 of 1 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

The post REBEL Core Cast 147.0–Ventilators Part 5: Key Mechanical Ventilator Pressures & Definitions Made Simple appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points + Don’t chase perfect numbers: Adequate and safe is often better than “perfect but harmful.” + Oxygenation levers: Start with FiO₂ and PEEP, but remember MAP is the true driver. + Ventilation levers: Adjust RR and TV, tailored to underlying physiology. + Watch your obstructive patients: Sometimes less RR is more*. Click here for Direct Download of the Podcast.

IntroductionVentilator management can feel overwhelming—there are so many knobs to turn, numbers to watch, and changes to make. But before adjusting any settings, it’s crucial to understand why the patient is in distress in the first place, because the right strategy depends on the underlying cause. In this episode, we’ll walk through three different cases to see how the approach changes depending on the problem at hand.

The 4 Main Ventilator Settings1. Tidal Volume (Vt) * Amount of air delivered with each breath * Typically set based on ideal body weight (6–8 mL/kg for lung protection) 2. Respiratory Rate (RR) * Number of breaths delivered per minute * Adjusted to control minute ventilation and manage CO₂ 3. FiO₂ (Fraction of Inspired Oxygen) * Percentage of oxygen delivered * Adjusted to maintain adequate oxygenation (goal SpO₂ 92–96%, PaO₂ 55–80 mmHg). 4. PEEP (Positive End-Expiratory Pressure) * Pressure maintained in the lungs at the end of exhalation to prevent alveolar collapse and improve oxygenation Modes of Ventilation1. AC/VC (Assist Control – Volume Control) * How it Works: Delivers a set tidal volume with each breath (whether patient- or machine-triggered). * When It’s Used / Pros: Most common initial mode; guarantees minute ventilation; good for patients with variable effort. * Limitations / Cons: May cause patient–ventilator dyssynchrony if set volumes don’t match patient’s demand. 2. AC/PC (Assist Control – Pressure Control) * How it Works: Delivers a set inspiratory pressure for each breath; tidal volume varies depending on lung compliance/resistance. * When It’s Used / Pros: Useful in ARDS (lung-protective strategy), limits peak airway pressures. * Limitations / Cons: Tidal volume not guaranteed; must closely monitor volumes and minute ventilation. 3. PRVC (Pressure-Regulated Volume Control) * How it Works: Hybrid: set target tidal volume, ventilator adjusts inspiratory pressure breath-to-breath to achieve it (within limits). * When It’s Used / Pros: Common default mode on newer vents; combines benefits of VC (guaranteed volume) + PC (pressure limitation). * Limitations / Cons: Can increase pressures if compliance worsens. 4. SIMV (Synchronized Intermittent Mandatory Ventilation) * How it Works: Delivers set breaths, but allows spontaneous patient breaths in between (without guaranteed volume). * When It’s Used / Pros: Used for weaning; allows patient effort. * Limitations / Cons: Risk of increased work of breathing if spontaneous breaths are inadequate. 5. PSV (Pressure Support Ventilation) * How it Works: Every breath is patient-initiated; ventilator provides preset pressure support to overcome airway resistance. * When It’s Used / Pros: Weaning trials; patients with intact drive who just need assistance. * Limitations / Cons: Not a full-support mode; not for unstable patients without spontaneous drive. Ventilation Strategies1. Airway Protection * Low GCS, seizure, stroke * Loss of gag/cough reflex * High aspiration risk (vomiting, GI bleed, poor mental status) 2. Hypoxemic Respiratory Failure * Severe pneumonia * ARDS * Pulmonary edema * Inhalation injury 3. Ventilatory (Hypercapnic) Failure / Increased Ventilation Demand * Severe metabolic acidosis (DKA, sepsis, renal failure) → need high minute ventilation * COPD, asthma (if decompensating) * Neuromuscular weakness (myasthenia, Guillain–Barré, spinal cord injury) 4. Airway Obstruction / Anticipated Loss of Airway * Tumor, anaphylaxis, angioedema * Facial or airway trauma * Pre-op / anticipated deterioration Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Show Notes Priyanka Ramesh, MDPGY 1 Internal Medicine ResidentCape Fear Valley Internal Medicine Residency ProgramFayetteville NCAspiring Pulmonary Critical Care FellowShowing Slide 1 of 1 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

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REBEL Rundown IntroductionWelcome to the Rebel Core Content Blog, where we delve into crucial knowledge for emergency medicine. Today, we share insightful tips from PEM specialist Dr. Elise Perelman, shedding light on respiratory challenges in infants, toddlers, and young children during the viral season. Understanding that most cases involve typical viruses, we aim to equip you with diagnostic pearls to identify more serious pathologies.

Click here for Direct Download of the Podcast.

Recognizing Respiratory PatternsPearl #1: Look at Your Patient

Begin exams from the doorway. Observing patterns such as accessory muscle usage can reveal a patient’s respiratory effort. Specify whether the work of breathing occurs during inspiration, expiration, or both. Inspiratory work indicates difficulty getting air in, while expiratory work suggests trouble pushing air out. Silent tachypnea may point to other issues, like acidemia or pneumothorax.

Localizing Sounds for Accurate DiagnosisPearl #2: Localize the Sound

Breathing noises signal varied respiratory issues. Stridor, often heard on inspiration, results from obstructions above the thoracic inlet. Conversely, wheezing, generally linked to exhalation, indicates obstructions in the lower airways. Watch for signs like ‘silent chest’—a dangerous, severe obstruction, and distinguish grunting as a bodily mechanism to prevent alveolar collapse. Correctly identifying the sound assists in determining the appropriate intervention.

Tailoring Treatment for Effective ResultsOnce a sound is localized, treatments vary. We explore Soder from nasal congestion, typically needing supportive care and suctioning. Stridor from conditions like croup is eased with interventions to reduce airway swelling, such as steroids or inhaled epinephrine. Conversely, wheezing in infants is often due to bronchiolitis—not bronchospasms—and over-treatment is to be avoided. Supportive measures including suction, hydration, and oxygen are preferred unless improvement warrants bronchodilators.

Intervening with Severe AsthmaIn severe cases of asthma or bronchiolitis, where standard at-home treatments fail, immediate adjunct therapies like intramuscular epinephrine become essential. Administering this quickly can alleviate obstruction when inhalants aren’t effective due to low air movement.

Navigating the Zebras of Respiratory CasesWhen recognizing Zebras—uncommon cases overshadowed by routine diagnoses—remain vigilant for histories or presentations that don’t conform. Conditions like pneumonia, bacterial tracheitis, and even myocarditis may mimic more common issues.

ConclusionAs attending physicians, our role extends beyond conventional treatment—it’s about discerning the atypical from the typical. Dr. Perelman urges continual reassessment, emphasizing reliance on observational skills as much as technological aid. Keeping keen on respiratory nuances ensures we catch those outlier cases, paving the way for adept medical care despite the overwhelming prevalence of viral infections.

Stay tuned for more pearls and insights in our future posts, as Dr. Perelman shares further strategies for effective pediatric emergency care. For more resources, continue exploring our faculty’s valuable contributions on our site. Until then, stay safe and perceptive in your practice.

Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO), and Marco Propersi, DO (X: @Marco_Propersi)

Guest###### Elise Perlman

MDPediatric Emergency Medicine​Assistant Professor, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell

Meet The Team Your Deep-Dive Starts Here###### REBEL Core Cast—Nitrous Oxide Toxicity: Whippets and Neurologic Injury

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REBEL RundownIntroductionWelcome to this special edition of the REBEL Cast, where we unravel key highlights and educational insights from the IncrEMentuM Conference in Spain. This event is a cornerstone for advancing emergency medicine education, drawing esteemed speakers and participants from around the globe. As emergency medicine gains traction in Spain, this conference has become an essential platform for knowledge exchange and professional growth. Today, host Dr. Mark Ramzy shines a spotlight on three distinguished speakers: Dr. Jess Mason, Dr. Tarlan Hedayati, and Dr. Simon Carley, who shared their expertise and experiences at this transformative gathering last spring.

Click here for Direct Download of the Podcast.

What's IncrEMentuM?A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals.

Pearls from Their IncrEMentuM 2025 Lectures Think about alternative diagnoses that could be driving the patient’s atrial fibrillation * Maybe the atrial fibrillation is an adaptive response and slowing them down (whether chemically or electrically) may cause more harm than good * Get in the mental space before having to perform a High Acuity Low Occurrence (HALO) procedure and walk through each of the parts step by step + - EMRAP has uploaded the video of the Resuscitative Hysterotomy here (Subscription required to watch)* + Like many things in critical care, a patient with a severe head injury requires you to do many little things very well (ie. reducing ICP increases by taking off the C-collar if able, positioning the patient appropriately, knowing when to use certain medications) See you in Spain!The upcoming conference aims to gather world-class educators once more and promises an enriching experience for all attendees. Drs. Tarlan Hedayati, Jess Mason and Simon Carley, along with many others, will be there at the event. For more information on the IncrEMentuM Conference and to register, visit their website! See you there!

Tarlan Hedayati, MDVice Chair of Education and Associate Program DirectorCook County, Chicago, IL * * Jess Mason, MDAssociate Professor of Emergency MedicineVanderbilt University, Nashville, TN Simon Carley, MD, PhDProfessor of Emergency and Dean of the Royal College of Emergency MedicineManchester, England * * * * Showing Slide 1 of 3 Your Deep-Dive Starts Here###### REBEL Core Cast 110.0 – On Shift Learning Pearls

Take Home Points: Patients with recent onset atrial fibrillation can ...

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REBEL Rundown Key Points + Prolonged QTc raises risk of torsades de pointes + Correct for heart rate: QTc > 440 ms (men) or > 460 ms (women); > 500 ms = high TdP risk. + Common culprits: Methadone, ondansetron, macrolides, fluoroquinolones, antipsychotics. + Prevention: Check & replete K, Mg, Ca and avoid QT-prolonging meds when possible. + If TdP develops: Defibrillate + IV magnesium* and stop offending agents. Click here for Direct Download of the Podcast.

IntroductionThe QT interval is a vital part of ECG interpretation, reflecting the heart’s electrical recovery after each beat. When prolonged, it can set the stage for torsades de pointes. Understanding how to measure and correct the QT interval, identify high-risk medications, and act quickly when TdP occurs is essential for every clinician. This guide walks you through the physiology, interpretation, common causes, and emergency management of QTc prolongation to keep your patients safe.

Definition and Physiology QT evaluation is a fundamental component of EKG analysis. The QT interval reflects the time from ventricular depolarization and contraction through ventricular repolarization and relaxation. * Clinically, QT prolongation increases the risk of torsades de pointes (TdP) – a form of polymorphic ventricular tachycardia (a non-perfusing rhythm) that is classically described as a pattern of “twisting points” or alternating amplitudes. This occurs when a premature ventricular contraction leads to an R on T phenomenon during the repolarization period. * The differential for QT prolongation is long and varied: congenital long QT, electrolyte disturbances (hypoK, hypoMg, hypoCa), hypothermia, myocardial ischemia, and increased intracranial pressure. Moreover, a whole host of xenobiotics can prolong the QT interval: methadone, anti-microbials, anti-emetics, anti-psychotics, and anti-dysrhythmics. ECG Interpretation The QT interval must be interpreted in conjunction with the patient’s heart rate. The QT interval with shorten in the context tachycardia and length in the context of bradycardia. In other words, tachycardia is protective when evaluating the patient with prolonged QT. * With that in mind, many EKG machines will calculate a corrected QT interval or QTc. The QTc is a standardized way to account for variations in heart rate so clinicians are able to compared QT intervals at different heart rates over time and thus calculate risk. * Generally, a QTc is considered prolonged if greater than 440ms in males or 460ms in females. Once the QTc > 500msec, the risk of TdP increases 2-3 fold.1 * A variety of different correction formulas exist: Bazett, Fridericia, Hodges, Framingham, Rautaharju. * Manually, the QT interval should be measured from the beginning of the QRS complex to the end of the T wave – and thus should be measured in leads where all portions can be visualized, most frequently lead II or V5/V6. Ideally, the QT interval should be average over 3 or more beats.2 To determine the end of the T wave, a tangent line should be drawn through the maximum slope of the T wave – the point at which this line crosses the isoelectric line is the end of the T wave.3 Commonly Used QTc Prolonging Medications Methadone: particularly concerning because not only does it inherently prolong QT but also induces a bradycardia * Antiemetics: Ondansetron * Macrolides: azithromycin, erythromycin, clarithromycin * Fluroquinolones: ciprofloxacin, levofloxacin * Antipsychotics: Haloperidol, Olanzapine Management Prevention is key! + Assess electrolytes (Mg, Ca, K) and replete as needed + Telemetry Monitoring * If patient happens to fall into TdP, initiate ACLS with immediate defibrillation and magnesium. * Withdrawal of offending agents. References1. Drew BJ, Ackerman MJ, Funk M, Gibler WB, Kligfield P, Menon V, Philippides GJ, Roden DM, Zareba W. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010 Mar;121(8):1047-1060. 2. Postema PG and Wilde AAM. The measurement of the QT interval. Curr Cardiol Rev. 2014 Aug;10(3): 287-294. 3. https://litfl.com/qt-interval-ecg-library/ Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Associate Editor###### Anand Swaminathan

MD, MPHAll Things REBEL EM

Meet The Team Your Deep-Dive Starts Here###### REBEL Cast Ep82: Timing of Endoscopy for UGIB

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Abdominal and GastrointestinalRead More###### REBEL Cast Ep 46b: Vent Management in the Crashing Patient with Haney Mallemat

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REBEL Rundown Key Points Tourniquets save lives and limbs: Apply immediately when you’ve got arterial bleeding. * Placement matters: Position the tourniquet 5–6 cm proximal to the arterial bleed, or if you can’t identify the exact source, place it as high up on the limb as possible. * Windlass technique: The windlass provides only a small amount of extra pressure. Tighten the velcro first, then twist the windlass 1–2 turns* to complete compression. Click here for Direct Download of the Podcast.

Highlights* 00:00 Introduction to Tourniquets * 00:40 Optimal Placement of Tourniquets * 01:21 Proper Tightening Techniques * 01:57 Importance of Timing and Application * 02:36 Summary and Conclusion IntroductionIn this episode of the Rebel Core Content podcast, Swami provides crucial tips on using tourniquets. Highlighting the significance of these life and limb-saving devices, the discussion focuses on the optimal placement of tourniquets, emphasizing placing them 2-3 inches (5-6 cm) above the bleeding source and avoiding joints. Swami also advises on the correct way to tighten the tourniquet using the Velcro strap first, followed by minimal use of the windless. The importance of noting the application time to avoid prolonged arterial flow interruption is also discussed. The episode concludes with a reminder to visit the podcast’s website for more valuable content.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Associate Editor###### Anand Swaminathan

MD, MPHAll Things REBEL EM

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REBEL RundownIntroductionIn this exciting episode of REBEL Cast, host Dr. Mark Ramzy joins forces with renowned educator and speaker, Dr. George Willis. Broadcasting straight from the ACEP 25 in Salt Lake City, the duo talk about bringing together the international emergency medicine community, as they reflect on their experiences at the Increment Conference in Murcia, Spain, and preview the upcoming event this spring.

Click here for Direct Download of the Podcast.

What's IncrEMentuM?A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals.

Pearls from George's IncrEMentuM 2025 Lectures:1. Sodium Bicarbonate Use: * Appropriate Use: Focus on specific instances like metabolic acidosis with renal failure or severe metabolic cases with tox patients (e.g., salicylate or TCA overdose). * Emphasis on Patient-Centric Care: Treat the patient, not the number; avoid harmful overreliance on bicarb based solely on lab results 2. Diabetic Ketoacidosis (DKA): * Balanced Solutions: Preferenced over normal saline to prevent hyperchloremic acidosis. * Potassium Management: Oral potassium is effective and should be utilized, challenging the myth of impaired gastric absorption in DKA. * Squid Protocol: Usage of ultra-rapid insulin subcutaneously as an alternative to insulin drips in mild to moderate DKA cases. * We covered this topic before on REBEL EM. Check out the post here and the podcast here 3. Crashing Aortic Dissection: * Hypotension Insights: Do not attribute sudden hypotension solely to medication; prioritize ruling out tamponade or cardiogenic shock. * Ultrasound Utilization: Essential tool for detecting complications like tamponade or low EF due to myocardial infarction or aortic valve regurgitation. * Controlled Pericardial Drainage: Crucial technique to stabilize hemodynamics without increasing mortality, avoiding extensive fluid removal. * Here’s a helpful algorithmic infographic to reference for aortic dissection patients: * Image Courtesy of Dr. Mark Ramzy, DO (@MRamzyDO) 4. Hyperkalemia

* Not every patient needs calcium. Dont just give it prophylatically, only those with EKG changes should get it and get enough of it.
* Give an appropriate dose of your other medications. That includes giving 10 units of insulin and 2 amps of dextrose 50. One when they get the 10 units of insulin and the other 30 minutes later
* Patients may be dehydrated, dont give them furosemide or diuretics. Those patients need fluid to help perfuse their kidneys and eliminate potassium
* Here’s the Algorithm George mentioned in the episode
* 
* Here’s a REBEL REVIEW breaking down the different electrolytes in each of the types of fluids:

Teasers from George's IncrEMentuM 2026 Lectures:1. Severe Thyroid Storm: * Diagnosis Reminder: Consider thyroid storm in febrile patients with altered mental status; order TSH tests. * Beta Blocker Administration: Use ultrasound to assess heart function before administering propranolol to prevent low output heart failure. * Medication Timing: Administer iodine after antithyroid drugs. 2. Refractory Hypoglycemia: * Early Use of Octreotide: Beneficial in sulfonylurea-induced cases; initiate treatment promptly for better efficacy. * Broadened Perspective: Consider other endocrine disorders as potential causes beyond typical measures. 3. Modern Management of SCAPE: * Bolus Dose Nitroglycerin: A recommended practice for quick patient stabilization and improved outcomes in SCAPE scenarios. * We covered this topic before on REBEL EM, see Dr. Marco Propersi’s post here See you in Spain!The upcoming conference aims to gather world-class educators once more and promises an enriching experience for all attendees. George Willis, along with many others, will bring significant discourse to the event. For more information on the IncrEMentuM Conference and to register, visit their website! See you there!

Mark Ramzy, DOCo-Editor-in-ChiefRWJBH / Rutgers Health, Newark NJ * George Willis, MDVice Chair and Assistant Program DirectorUT Health, San Antonio, TX Showing Slide 1 of 2 Your Deep-Dive Starts Here###### REBEL Core Cast – DKA: Beyond the Basics Part 2 – SCOPE DKA-Trial

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Endocrine, Metabolic, Fluid, and ElectrolytesRead More###### REBEL Core Cast 18.0 – DKA Tips and Tricks

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Endocrine, Metabolic, Fluid, and ElectrolytesRead MoreShowing Slide 1 of 4The post REBEL CAST – IncrEMentuM26 Speaker Spotlight : George Willis and Mark Ramzy appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL RundownKey Points Fluid Choice Matters: Plasma-Lyte, a balanced crystalloid, corrected acidosis faster than normal saline in severe DKA patients, with no increase in adverse events. * Chloride Load Concerns: Normal saline’s high chloride content can worsen acidosis, potentially slowing bicarb recovery even after the anion gap closes. * Study Design Strengths: The SCOPE-DKA trial was a cluster crossover, open-label RCT, protocolizing all variables except fluid type, enhancing the reliability of its findings. * Base Excess & Strong Ion Difference: Base excess/deficit and strong ion difference are valuable but underutilized tools for assessing acid-base status—don’t rely solely on pH or bicarb. * Limitations & Next Steps:* The study did not include lactated Ringer’s, and fluid rates were left to clinical discretion. More research, including three-arm trials, is needed for definitive guidance. Click here for Direct Download of the Podcast.

IntroductionManaging diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, especially in severe cases. In part two of our REBEL Cast DKA series, we shifted from insulin strategies to fluid choice in severe DKA, diving into the SCOPE-DKA trial—a cluster, crossover, open-label RCT from Australia. While normal saline (NS) is commonly used, concerns about its high chloride content and impact on acidosis have sparked growing interest in balanced solutions like Plasma-Lyte.

Clinical QuestionDoes the fluid you choose affect how quickly acidosis resolves in DKA?

IV Fluid Composition Clinical Bottom LinePlasma-Lyte showed a modest but meaningful benefit over normal saline in resolving metabolic acidosis in patients with severe DKA. Though safety profiles were similar, the more balanced electrolyte composition of Plasma-Lyte helped normalize acid-base status slightly faster—without worsening ketosis. While this won’t revolutionize care overnight, it’s one more step toward physiologic resuscitation in DKA. Understanding fluid composition and its impact on acid-base balance is crucial for optimal patient care.

Post Peer Reviewed By: Marco Propersi (Twitter/X: @Marco_propersi), and Kim Bambach, MD

Show Notes By: Mark Ramzy, DO

Authors Mark Ramzy, DOCo-Editor-in-ChiefRWJBH / Rutgers Health, Newark, NJ Frank LodesertoAssociate EditorCape Fear Valley Medical Center,Fayetteville NCShowing Slide 1 of 2 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

REBEL Castis the blogs audio version. The podcast typically starts by setting a clinical stage with a pertinent clinical question, followed by a discussion of the paper with pertinent results, strengths, limitations, and further discussion. Finally, we end every podcast with clinical take home points from the papers being reviewed. If there are papers you think we should evaluate, email them to srrezaie@gmail.com.

REBEL EM stands for Rational Evidence Based Evaluation of Literature in Emergency Medicine. We cover a myriad of topics, primarily focusing on evidence-based clinical topics.

At its core, evidence-based medicine (EBM) incorporates clinical judgment, relevant scientific evidence, and patient values/preferences. Research and scientific evidence help inform care but should not dictate care of patients.

With the constant influx of new published research, it makes it difficult to stay current with the latest and greatest. REBEL EM was created October 2013 in an effort to cut down knowledge translation of research to clinical application (Bench to Bedside), using a structured critical appraisal method of evaluation.

REBEL Core Cast – DKA: Beyond the Basics Part 2 – SCOPE DKA-TrialMark RamzyOctober 21, 2025No CommentsManaging diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, especially in severe cases. In part two of our REBEL Cast DKA series, we shifted from insulin strategies to fluid choice in severe DKA, diving into the SCOPE-DKA trial—a cluster, crossover, open-label RCT from Australia. While normal saline (NS) is commonly used, concerns about its high chloride content and impact on acidosis have sparked growing interest in balanced solutions like Plasma-Lyte.

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REBEL Rundown Key Points Fewer ICU Admissions
Only 5 patients in the SQuID group required ICU care vs 99 in the traditional insulin drip group. * Shorter ED Stays
ED length of stay dropped by ~3 hours in the SQuID group—an operational win in crowded departments. * No Drop in Nursing Workload
Despite using subQ insulin, nurses still performed hourly glucose checks and frequent injections. * Focus on the Anion Gap
DKA resolution = closing the anion gap, not just normalizing blood sugar—critical concept for trainees and nurses alike. * Peds Has the Edge*
Pediatric ICUs routinely use a 2-bag system (D10 + electrolytes vs electrolytes alone) to safely continue insulin while managing glucose—adult medicine should take note. Click here for Direct Download of the Podcast.

IntroductionIn this episode of REBEL Cast, we dive into part one of our Diabetic Ketoacidosis (DKA) series with a twist—subcutaneous insulin instead of the traditional IV drip. We explore the SQuID Protocol (Subcutaneous Insulin in DKA), which could potentially shift how we manage mild to moderate DKA—from the ICU to the general floor.

With ICU bed shortages, ED boarding, and nursing resource challenges, it’s time to ask: Do all DKA patients really need a drip and an ICU bed?

We reviewed a quasi-experimental study comparing traditional insulin drips versus subcutaneous insulin (lispro q4h + glargine at time zero) in a busy urban ED. The results? Promising—but not without caveats.

SQuID Protocol Clinical Bottom LineThe SQuID Protocol appears safe and effective for carefully selected patients with mild to moderate DKA. It may reduce ICU admissions and shorten ED stays. But implementation requires thoughtful coordination, nursing comfort, and institutional buy-in. This isn’t ready for prime time everywhere—but it’s worth knowing and considering when ICU resources are tight.

Post Peer Reviewed By: Marco Propersi (Twitter/X: @Marco_propersi), and Kim Bambach, MD

Show Notes By: Mark Ramzy, DO

Authors Mark Ramzy, DOCo-Editor-in-ChiefRWJBH / Rutgers Health, Newark, NJ Frank LodesertoAssociate EditorCape Fear Valley Medical Center,Fayetteville NCShowing Slide 1 of 2 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

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REBEL Rundown Key Points + Don’t chase perfect numbers: Adequate and safe is often better than “perfect but harmful.” + Oxygenation levers: Start with FiO₂ and PEEP, but remember MAP is the true driver. + Ventilation levers: Adjust RR and TV, tailored to underlying physiology. + Watch your obstructive patients: Sometimes less RR is more*. Click here for Direct Download of the Podcast.

IntroductionWhen you take the airway, you take the wheel and you now control the patient’s oxygenation and ventilation. In this REBEL Crit episode, Dr. Lodeserto and Dr. Acker walk through the physiology, ventilator strategies, and clinical curveballs that separate calm control from chaos at the bedside.

The Two Pillars of Vent Management1. Oxygenation — Getting O₂ In

• Primary levers: FiO₂ (fraction of inspired oxygen) and PEEP (positive end-expiratory pressure).
• Real driver: Mean Airway Pressure (MAP) : the average pressure applied to the lungs across the entire respiratory cycle.
• Key physiology:
  • Oxygen enters blood by diffusion down a concentration gradient.
  • Adequate alveolar surface area is critical → PEEP keeps alveoli open, prevents collapse/reopen injury, and ensures FiO₂ delivery actually translates into effective oxygenation.
• MAP analogy: Just as mean arterial pressure drives perfusion, mean airway pressure drives oxygenation. Prolonged inspiratory time or sustained pressure (e.g., APRV, inverse I:E) can raise MAP.
• Risks: Excessive pressure/volume can cause barotrauma or volutrauma.

2. Ventilation — Getting CO₂ Out

• Primary levers: Tidal Volume (TV) and Respiratory Rate (RR).
• Minute Ventilation = RR × TV.
• Mechanism: Ventilation removes CO₂ through bulk convection (movement of air in and out).

Disease-specific strategies:

• Obstructive Disease (COPD / Asthma)
  • RR ↓ to allow more time for exhalation.
  • Ensure expiratory flow = inspiratory flow → prevents air trapping.
  • If not equal → auto-PEEP → increased intrathoracic pressure → ↓ preload, risk of hypotension, cardiac arrest, or pneumothorax.
• Metabolic Acidosis
  • RR ↑ to blow off CO₂ and buffer acidosis.
• ARDS
  • Tidal volume limited to 4–6 mL/kg IBW to minimize ventilator-induced lung injury.
  • RR becomes the main adjustment knob.
  • Exception: in obstructive lung disease, patients need extra time to exhale (I:E may be 1:4–1:6). Why This MattersVentilator management is part science, part art. Understanding the physiology and knowing when to bend or break the rules helps protect patients from ventilator-induced injury and improves outcomes.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Show Notes By: Rubén Tapia-Bucheli, M.D.

Guest Contributors Rubén Tapia-Bucheli, M.D.3rd Year Internal Medicine ResidentCape Fear Valley Internal Medicine Residency ProgramFayetteville NCAspiring Pulmonary Critical Care FellowShowing Slide 1 of 1 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

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REBEL Rundown Key Points Start with Breath Types: Controlled, assisted, and supported breaths are the foundation of all modes. * Comfort Over “Best Mode”: No mode improves mortality — focus on patient synchrony and comfort. * Know the Big 5 Modes: AC: All controlled or assisted (volume or pressure). PS: Fully spontaneous, great for SBTs. PRVC: Pressure-delivered, volume-targeted hybrid. SIMV: Mixed mode, less favored in adults. VS: Spontaneous mode with adaptive pressure. * Watch for Pitfalls: PRVC may under-ventilate in agitation. SIMV often causes dyssynchrony. * Bottom Line:* Master mode mechanics and match the vent to the patient — not the other way around. Click here for Direct Download of the Podcast.

IntroductionMechanical ventilation can feel overwhelming, especially when faced with a sea of ventilator modes and unfamiliar terminology. In Part 2 of the series, we go beyond breath types and delivery mechanics to explore the most used modes in the ICU. We will break down each one; explaining how it works, when to use it, and why the goal isn’t the “best mode” but the most comfortable one for the patient.

Ventilator Modes Explained Assist Control (AC)

• Commonly mislabeled as “volume control” or “pressure control.”
• Two main types:
  • AC Volume: Delivers a preset tidal volume with each breath, whether machine-initiated (controlled) or patient-initiated (assisted).
  • AC Pressure: Delivers a preset pressure; tidal volume varies based on compliance.
• All breaths are either controlled or assisted.

Pressure Support (PS)

• All breaths are spontaneous initiated by the patient.
• The ventilator provides a preset level of pressure support, like a resistance band during a pull-up.
• No set rate, but a backup mode (often AC) activates during apnea.
• Commonly used for spontaneous breathing trials (SBTs) to assess extubation readiness.
  • Typical goal: Patient breathing comfortably with PS ~5 cmH₂O and reasonable rate.

Pressure Regulated Volume Control (PRVC)

• Also called autoflow or adaptive pressure ventilation.
• A hybrid mode: Pressure-delivered, volume-targeted.
• Delivers breaths with a decelerating flow waveform, mimicking physiologic breathing.
• Adjusts pressure breath-to-breath to meet a target tidal volume with minimal required pressure.
• Safety feature: Pressure limit (e.g., 30–35 cm H₂O). If exceeded, volume delivery stops early.
• Pitfall: In agitated patients, rapid breathing may trick the ventilator into reducing pressure, causing under-ventilation.

Synchronized Intermittent Mandatory Ventilation (SIMV)

• Less common in adult ICU but still commonly used in pediatrics.
• Delivers a set number of mandatory (controlled or assisted) breaths.
• Allows spontaneous, pressure-supported breaths between mandatory ones.
• Example: SIMV 10 = 10 guaranteed AC breaths; additional breaths are spontaneous + supported.
• Why it’s less popular: Found to be less effective than daily SBTs for weaning and frequent dyssynchrony from not giving enough PS (PS should target at least 2/3 of the AC breath volumes) .

Volume Support (VS)

• A newer, fully spontaneous mode (like PS + PRVC).
• Patient initiates all breaths.
• The ventilator automatically adjusts pressure support to achieve a target tidal volume.

• Think of it as the spontaneous cousin of PRVC—adaptive and volume-driven. Clinical Bottom LineUnderstanding ventilator modes starts with knowing breath types, delivery mechanics, and clinical goals. When it comes to choosing the right mode:

• Focus less on the “best” mode and more on patient comfort and synchrony.

• Recognize the strengths, limitations, and pitfalls of each mode.
• Stay tuned for future episodes that dive into ventilator troubleshooting and advanced respiratory strategies. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Show Notes By: Nicole Ebalo, DO

Guest Contributors Eric Acker, MDInternal Medicine, Chief Resident,Cape Fear Valley Medical Center,Fayetteville NC Nicole Ebalo, DOInternal Medicine, Chief Resident,Cape Fear Valley Medical Center,Fayetteville NCShowing Slide 1 of 2 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

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REBEL RundownClick here for Direct Download of the Podcast.

Highlights* 00:00 Introduction to Rebel Cast * 00:10 Highlighting the Incrementum Conference 2026 * 00:34 Meet the Founders of Incrementum * 01:21 The Journey to Incrementum * 04:27 The Recognition of Emergency Medicine in Spain * 06:04 What is Incrementum? * 08:14 Bringing Together Top Emergency Medicine Experts * 11:38 Exciting Sessions to Look Forward To * 15:54 Conclusion and Invitation to Incrementum 2026 IntroductionIn this special episode of Rebel Cast, we spotlight the Incrementum Conference in Spain, a significant event in emergency medicine. Hosts welcome Dr. Francisco ‘Paco’ Campillo Palma and Dr. Carmen Maria Cano, founders of Incrementum, to discuss the recognition of emergency medicine as a specialty in Spain. They share their journey of creating the conference, emphasizing the importance of education, collaboration, and growth. The discussion also touches on this year’s conference highlights, including sessions on mental health and evidence-based medicine, and the exceptional lineup of speakers. Listeners are encouraged to attend the conference in April 2026 for an enriching experience.

Bottom Line Join us in Spain this April for the Increment Conference! * Register now at incrementum-conference.com Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO)*

Co-Editor-In-Chief###### Marco Propersi

DOAll Things REBEL EM

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REBEL Rundown Key Points + Master the 3 Types of Breaths
Control, Assist, and Spontaneous — know the difference before tackling ventilator modes. + Breath Delivery: Volume vs. Pressure
Volume-Targeted = fixed volume → monitor pressure
Pressure-Targeted = fixed pressure → monitor volume + Lung Compliance = Pressure-Volume Relationship*
Volume mode: ↑ pressure = ↓ compliance (stiff lungs)
Pressure mode: ↓ tidal volume = ↓ compliance Click here for Direct Download of the Podcast.

IntroductionFor many medical residents, the ICU can feel like stepping into a pressure cooker. At the heart of that stress often lies one intimidating machine: the ventilator. Rather than diving headfirst into complex ventilator modes, this episode lays a critical foundation by breaking down the basic building blocks of mechanical ventilation, something every clinician should master before moving on to more advanced concepts. Once you know the 3 types of breaths and how those breaths are delivered, you can more easily understand most of the mechanical ventilator modes.

The 3 Types of BreathsTo simplify things, we use a pull-up analogy to explain the types of ventilator breaths:

The 3 Types of Breaths…It's Like Breath Delivery: Volume vs. Pressure Once you know the type of breath, the next key concept is how* it’s delivered:

1. Volume-Targeted Delivery

+ The ventilator delivers a fixed **tidal volume** (e.g., 400 mL) with each control or assist breath.
+ **What to monitor:** **Pressure.** As lung compliance worsens, pressure increases.
+ **Risk:** Barotrauma if the pressure becomes too high.**2. Pressure-Targeted Delivery**


+ The ventilator delivers air to a preset **pressure** (e.g., 15 cm H₂O).
+ **What to monitor:** **Tidal volume.** As compliance drops, so does delivered volume.
+ **Adjustment:** Modify pressure to maintain appropriate ventilation.

Putting It All Together: Lung Compliance The relationship between pressure and volume is described by compliance: + Compliance = Δ Volume / Δ Pressure * In volume mode: + Rising pressure to achieve the same volume = decreased compliance (stiff) + Decreasing pressure to achieve the same volume = increased compliance (loose) * In pressure mode:* + Dropping tidal volume at a constant pressure = decreased compliance (stiff) + Rising tidal volume at a constant pressure = increased compliance (loose) Clinical Bottom LineBefore tackling advanced ventilator modes, master these foundational concepts:

• The three breath types
• The two delivery methods
• The role of lung compliance

Once you’ve got these down, the rest of mechanical ventilation becomes far easier to understand.

Stay tuned for Part 2, where we’ll build on this foundation and unpack the most commonly used ventilator modes.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Show Notes By: Nicole Ebalo, DO

Guest Contributors Eric Acker, MDInternal Medicine, Chief Resident,Cape Fear Valley Medical Center,Fayetteville NC Nicole Ebalo, DOInternal Medicine, Chief Resident,Cape Fear Valley Medical Center,Fayetteville NCShowing Slide 1 of 2 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

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REBEL Rundown Key Points IO Lines Are Life-Saving in Extremis: IO access is fast, reliable, and can deliver nearly any resuscitative medication or fluid during cardiac arrest or hemorrhagic shock. * Location Matters for Flow. Sternal IO: Fastest (up to 500cc/5 min). Humerus IO: Faster than tibia (300cc/5 min). Tibial IO: Slower (200cc/5 min) but easier to place during CPR * Watch for Contraindications: Avoid IO placement in bones with fractures, prior IO attempts, or compromised circulation proximal to the site. * Labs From IO = : Labs drawn from IO lines are generally unreliable. Once stabilized, obtain bloodwork through IV access. * Stabilize or Lose It: IO dislodgement is common—always use a stabilizer or secure with gauze and tape if none is provided. * Don’t Forget Non-Trauma Uses:* IO isn’t just for trauma—think about it in medical arrests, shocked pediatric patients, and patients with difficult IV access. Click here for Direct Download of the Podcast.

Highlights* 00:00 Introduction to the Podcast * 00:07 First Encounter with Intraosseous Lines * 01:09 Advantages of Intraosseous Lines * 02:42 Intraosseous Lines in Pediatric Patients * 03:34 Optimal Locations for Intraosseous Lines * 06:17 Limitations and Considerations * 07:34 Conclusion and Final Thoughts IntroductionWelcome to the Rebel Core Content blog, your go-to source for core medical concepts applicable to practitioners anywhere, anytime. Today, we delve into the world of Intraosseous (IO) lines—a crucial tool in emergency medicine. Swami shares insights into the effectiveness and limitations of IO usage in diverse clinical scenarios.

BackgroundThe sicker the patient, the more likely an IO line is the right choice. In emergencies such as cardiac arrest or hemorrhagic shock, the speed and reliability of IO access outshine traditional intravenous (IV) or central line placements. There’s virtually no resuscitation medication or blood product that cannot be administered through an IO, making it indispensable in life-threatening situations.

Location While proximal humerus site portents faster infusion rates than proximal tibia site, the main limitation of the proximal humerus site is that the arm must be held in internal rotation to avoid dislodgement of the IO * Proximal tibia may be easier to landmark than proximal humerus * Other sites include distal tibia, distal femur and sternum but are uncommonly employed in EDs Flow Rates Proximal Humerus IO + ~300cc over 5 minutes + Faster than tibia + May be harder to access in some trauma or positioning scenarios * Tibial IO + ~200cc over 5 minutes + Slower flow compared to humerus + Easier to access, especially during CPR or transport * Sternal IO + Up to 500cc over 5 minutes + Highest flow rate + Best for rapid volume resuscitation + Risk of dislodgement or interfering with CPR compressions Limitations* Placing an IO in a bone with a proximal fracture, a previous IO placement attempt or any circulatory compromise proximal to the site is contraindicated * Blood work drawn from an IO are generally not accurate, so once the patient has been resuscitated with the IO, intravenous blood draws are recommended * Dislodgement is common; it is best to use the stabilizer that comes with the IO kit; if the kit does not have a stabilizer, stack lots of gauze on both sides of the IO needle and tape it down Clinical Bottom LineIntraosseous lines are a powerful tool, particularly in acute resuscitation scenarios involving cardiac arrest or severe trauma. While they offer quick and effective access, Clinicians must remain vigilant about their limitations and be prepared to switch to more stable options as patients stabilize.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Associate Editor###### Anand Swaminathan

MD, MPHAll Things REBEL EM

Meet The Team Your Deep-Dive Starts Here###### REBEL Cast Episode 24: Advice to the Graduating Resident – Amal Mattu

So this is the second installation of Advice to Graduating ...

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CardiovascularRead More###### REBEL Cast Episode 17: The All Thoracotomy Episode

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REBEL Rundown Key Points Think Beyond Trauma: Don’t forget to suspect tension pneumothorax in ventilated patients who suddenly crash or after a central line placement! * Confirm with Ultrasound: If the patient is stable enough, grab the probe! Ultrasound can rapidly confirm tension PTX and avoid unnecessary delays. * Needles Are Out: Needle decompression? Meh. Finger thoracostomy* is faster, more reliable, and more definitive. Click here for Direct Download of the Podcast.

IntroductionOn this episode of the Rebel Core Cast, Swami takes a deep dive into pneumothorax decompression, focusing on the need for improvements beyond the classic teachings. Covering scenarios where immediate decompression is critical, particularly in tension pneumothorax, Swami discusses the limitations of needle decompression, especially in the second intercostal space at the midclavicular line. He highlights the importance of using POCUS for diagnosis and recommends skipping needle decompression in favor of finger thoracostomy for a more reliable and effective treatment. Key takeaways emphasize recognizing tension pneumothorax in various clinical situations and the advantages of finger thoracostomy over traditional techniques.

Highlights 00:00 Introduction to Pneumothorax Decompression * 00:17 Recognizing Tension Pneumothorax * 01:00 Common Scenarios for Pneumothorax * 01:34 Confirming Diagnosis with POCUS * 01:50 Issues with Needle Decompression * 03:21 Advantages of Finger Thoracostomy * 04:11 Key Takeaways and Conclusion References1. Ferrie EP et al. The right place in the right space? Awareness of site for needle thoracentesis. Emerg Med J 2005; 22: 788-9 PMID: 16244336 2. Laan DV et al. Chest wall thickness and decompression failure: a systematic review and meta-analysis comparing anatomic locations in needle thoracostomy. Injury; 2016; 47(4): 797-804 PMID: 26724173 3. Terboven T et al. Chest wall thickness and depth to vital structures in paediatric patients – implications for prehospital needle decompression of tension pneumothorax. Scan J Trauma Resusc Emerg Med 2109; 27(1). PMID: 30992028 Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)*

Associate Editor###### Anand Swaminathan

MD, MPHAll Things REBEL EM

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REBEL Rundown Key Points + Shock is a Clinical Diagnosis — Not Just a Number
Patients can be in compensated shock with normal BP. Look for signs like AMS, cool extremities, ↓ UOP, and ↑ HR/RR. + Start with the 4 L’s
Lucid (mental status), Limbs (warm/cold), Leak (urine output), and Lactate give you rapid bedside insight into perfusion status. + Pulse Pressure Helps Pinpoint the Type - Narrow PP = Cardiogenic, Hypovolemic, or Obstructive shock - Wide PP = Distributive shock (Sepsis, Anaphylaxis, Neurogenic) + Be Systematic at the Bedside*
Quick vitals, focused history, and targeted exam can reveal the etiology faster than invasive tools. Click here for Direct Download of the Podcast.

IntroductionIn this episode, we will dive into a simple yet effective bedside approach to a patient in shock. By using quick physical exam findings and bedside vitals (particularly pulse pressure), you can form a quick assessment of the likely underlying etiology of a critically ill patient.

Key ConceptsWhat is Shock? + - Supply vs. Demand mismatch: * Inadequate perfusion relative to metabolic demands * Leading to tissue hypoxia and cell death - DO2 = CO x (Hb x Sat + (0.003 x paO2)) * CO = Heart Rate x Stroke Volume * Determinants of Stroke Volume: Preload, Contractility, and Afterload - 4 L’s of Hypotension * Lucid: What’s their mental status? * Limbs: Are they cold vs. warm? What is the cap refill? * Leak: Are they taking a “leak”? What is the urine output? * Lactate - Remember: * Shock DOES NOT equal hypotension * A patient in shock can still have normotensive pressures in “Compensated Shock” - Signs of Shock * Increased HR, increased RR, AMS, decreased urine output, cool to touch, weak pulses, slow capillary refill Defining Blood Pressure1. * Systolic Blood Pressure + Stroke Volume: Main contributor to SBP SV ≈ SBP + Aortic/Arterial Compliance * Diastolic Blood Pressure + Systemic Vascular Resistance + Maintains end-organ perfusion in diastole * Pulse Pressure + SBP – DBP * Mean Arterial Pressure + MAP < 60-65 can lead to end-organ damage Narrow Pulse Pressure * Cardiogenic: “Cold Shock” + Low contractility low SV low SBP increased HR + increased SVR due to catecholamine release leading to increased DBP + Cold limbs, weak pulses, poor capillary refill * Hypovolemic + Hemorrhagic vs. Dehydration + Decrease preload decreased SV decreased SBP increased HR + increased SVR due to catecholamine release leading to increased DBP * Obstructive + - “Obstruction of preload” decreased SV low SBP increased HR + increased SVR due to catecholamine release leading to increased DBP - Pneumothorax * Increased intrathoracic pressure decrease IVC and SVC decreased preload - Cardiac Tamponade * Fluid in pericardial space decrease filling decreased preload * Pulmonary Emboli: Obstruction of RV to LA flow decreased preload Wide Pulse Pressure: Distributive Shock + “Warm shock”: Vasodilatation decreased SVR Decreased DBP + Septic: Main cause of distributive shock + Neurogenic: Loss of sympathetic tone unopposed parasympathetic / vagal tone decreased SVR decreased DBP + Anaphylaxis: histamine and other inflammatory mediators released increased vascular permeability decreased SVR decreased DBP + Adrenal Crisis: Not secreting cortisol not increasing vascular tone decreased SVR decreased DBP + Hepatic Failure: Increase in NOS increases NO vasodilatation Practical Bedside Approach When called to bedside: + Is the patient meeting any of the 4 “L’s” ? + Check the pulse pressure along with other vitals + Why are they here? What’s the brief history? * Narrow Pulse Pressure? Cardiogenic, hypovolemic, or obstructive shock * Wide Pulse Pressure? Distributive shock* + Think: sepsis (most likely), neurogenic, anaphylaxis, adrenal crisis, hepatic failure Clinical Bottom LineA brief but thorough bedside exam remembering the 4 “L’s”, a quick history, and examining the pulse pressure can help a clinician form a quick differential into the underlying etiology for a critically ill patient in shock. Stay sharp, stay systematic!

Shock is a clinical diagnosis based on bedside findings — not just blood pressure readings.

You don’t always need invasive monitoring to identify shock. Look at HR, RR, UOP, and mentation.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Guest Contributors Eric Acker, MDInternal Medicine Resident, Rising Chief Resident,Cape Fear Valley Medical Center,Fayetteville NC Micheal Bass DOInternal Medicine Resident, Rising Chief ResidentCape Fear Valley Medical Center,Fayetteville NC Frank J. Lodeserto MDAssociate Professor and Internal Medicine Residency Program DirectorAdult & Pediatric Critical Care Medicine, Cape Fear Valley Medical Center, Fayetteville, NCShowing Slide 1 of 3 Your Deep-Dive Starts Here###### REBEL Core Cast 144.0: Tourniquet Tips

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ToxicologyRead MoreShowing Slide 1 of 7The post REBEL Core Cast 138.0: A Simple Bedside Approach to Shock appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Rundown Key Points + Sinus Tachycardia = Clinical Clue: Don’t just treat the number—it’s a sign of underlying physiologic stress. + Oxygen Delivery Equation: HR ↑ may compensate for ↓ hemoglobin, O₂ sat, or cardiac output. Know: DO₂ = CO x Hb x Sat + 0.003(pO₂) + Systematic 8-Point Evaluation: Airway/Hypoxia, Breathing , Circulation, Drugs, Erythrocytes (Anemia), Fever, Glucose, “Holy Cow That Hurts” + Think Holistically: Tachycardia isn’t the problem—what’s causing it is. + Avoid Reflexive Beta Blockers: Don’t suppress a compensatory response before finding the cause. + Reassess Frequently:* Clinical status can change—stay vigilant. Click here for Direct Download of the Podcast.

IntroductionSinus tachycardia is the most prevalent cardiac dysrhythmia in critically ill patients, yet it often receives less attention than it warrants. While the rhythm itself is not inherently dangerous, it serves as a crucial indicator of underlying physiological disturbances that require prompt evaluation and management.

Key Concepts Sinus Tachycardia as a Clinical Sign: Rather than focusing solely on the elevated heart rate, clinicians should interpret sinus tachycardia as a symptom pointing toward an underlying cause that needs to be identified and addressed. * Oxygen Delivery Equation: Understanding the components of oxygen delivery—hemoglobin concentration, oxygen saturation, and cardiac output—is essential. An increase in heart rate may be a compensatory mechanism to maintain adequate oxygen delivery when other components are compromised. 8 Causes of Sinus Tachycardia1. Airway/Hypoxia: Ensure the airway is patent and assess for hypoxemia. 2. Breathing: Evaluate for respiratory distress or pulmonary pathology. 3. Circulation: Consider shock states, including hypovolemia, hemorrhage, or distributive shock. 4. Drugs: Review medications and substances that may cause tachycardia, including stimulants and withdrawal states. 5. Erythrocytes (Anemia): Assess for low hemoglobin levels that may impair oxygen delivery. 6. Fever: Recognize that fever increases metabolic demand, leading to tachycardia. 7. Glucose: Identify hypoglycemia or hyperglycemia as potential contributors. 8. Holy Cow That Hurts: (Pain/Anxiety): Acknowledge that pain and emotional distress can elevate heart rate. Practical Bedside Approach Holistic Assessment: Always interpret sinus tachycardia within the broader clinical context. * Avoid Reflexive Treatment: Refrain from immediately administering rate-controlling medications without identifying and managing the underlying cause. * Continuous Monitoring: Regularly reassess the patient’s status, as the underlying cause of tachycardia may evolve over time. Clinical Bottom LineSinus tachycardia is a vital clinical sign that necessitates a thorough and systematic evaluation to uncover and treat the root cause. By adopting this structured approach, clinicians can improve patient outcomes and avoid the pitfalls of symptomatic treatment without addressing underlying issues.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Guest Contributors Eric Acker, MDInternal Medicine Resident, Rising Chief Resident,Cape Fear Valley Medical Center,Fayetteville NC Thirumala “Keerthi” Kammaripalle, MDInternal Medicine Resident, Rising Chief ResidentCape Fear Valley Medical Center,Fayetteville NCShowing Slide 1 of 2 Your Deep-Dive Starts HereIt seems we can't find what you're looking for.

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REBEL Rundown Key Points + Short + shallow: Neuromuscular, bronchospasm, or compliance problem → act fast + Normal/large tidal volume: Compensation for metabolic/systemic cause + Use all tools*: Eyes: Chest rise, Hands: Palpate, Ears: Listen, Brain: Synthesize Click here for Direct Download of the Podcast.

IntroductionIn this episode, we focus on the bedside evaluation of the tachypneic patient. Tachypnea (increased respiratory rate) can be an early indicator of serious illness, but not every tachypneic patient is on the verge of arrest. The key is honing your bedside assessment to recognize who is at risk for rapid deterioration and why. We break down a practical approach you can use immediately at the bedside.

Key ConceptsFirst Priorities at the Bedside Chest Rise: + Short, shallow respirations with poor chest rise are a major red flag. + Patients with minimal tidal volumes are often approaching respiratory failure. * Diaphoresis and Tachycardia: + Diaphoresis + tachycardic patients with shallow breathing demand urgent attention as this is a sign of high catecholamine surge and impending respiratory collapse. * Immediate Action: + Use your eyes (chest rise), your ears (stethoscope), and brain (putting together all of the pieces together) Short, Shallow Breathing: Think Three Major Buckets1. Neuromuscular Disease * Myasthenia gravis crisis, Guillain-Barré, myopathies, frailty. * Weak inspiratory effort leads to low tidal volumes. * Needs urgent positive pressure support (BiPAP, or intubation). 2. Severe Bronchospasm * Asthma, COPD, anaphylaxis. * Shallow, forced expirations signal airway obstruction. * Silent Chest = airway emergency. + Treat with bronchodilators, steroids, and positive pressure ventilation. + Avoid immediate intubation if reversible; trial NIPPV first. 3. Worsening Lung Compliance * + - “Stiff lungs” harder to ventilate. - Compliance (C) = Δ Volume / Δ Pressure - So if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is low - Causes include: * Chest Wall: Rigidity, burn eschar. * Pleural Space: Effusion, pneumothorax (check for asymmetric chest rise). * Lung Parenchyma: Pneumonia, contusion, atelectasis. * Below the Lung: Abdominal distension, ascites. - Clinical pearl: Work outside-in (chest wall, pleura, lung, abdomen). Normal to High Tidal Volumes with Tachypnea: Systemic Causes1. Metabolic Acidosis (e.g., DKA) * Compensatory hyperventilation (Kussmaul breathing) * Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosis 2. Respiratory Alkalosis * Causes: Pain, anxiety, fever, early sepsis, CNS issues * Central drive increases respiratory rate * Again, ABG or VBG helps confirm 3. Dead Space Ventilation * Pulmonary embolism (PE) is the classic cause. * Other causes include: + Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow. + Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli. + Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but under perfused areas. + Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation * Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch. Practical Bedside Approach Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issue + Think: Impending respiratory failure, act quickly. * Normal to large tidal volumes? Systemic causes + Think: Compensation (acidosis, pain, anxiety, PE). * Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize). Clinical Bottom LineA careful, simple bedside assessment can rapidly identify which tachypneic patients need immediate intervention—and help you avoid missing those headed toward respiratory collapse. Stay sharp, stay systematic!

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Guest Contributors Eric Acker, MDInternal Medicine Resident, Rising Chief Resident,Cape Fear Valley Medical Center,Fayetteville NC Micheal Bass DOInternal Medicine Resident, Rising Chief ResidentCape Fear Valley Medical Center,Fayetteville NCShowing Slide 1 of 2 Your Deep-Dive Starts Here###### REBEL Core Cast 127.0 – Penetrating Neck Injuries

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REBEL Rundown Key Points + Hypoxemia = low blood oxygen + Hypoxia = low tissue oxygen + 5 causes of hypoxemia, but most hospital cases are either: - Shunt = doesn’t improve with oxygen therapy - Dead space = causes tachypnea but is easier to oxygenate + Always start with maximizing oxygen delivery (),
but recognize quickly when positive pressure () is needed + V/Q mismatch + Shunt* (refractory to oxygen therapy) Click here for Direct Download of the Podcast.

IntroductionIn this episode, we break down a practical bedside approach to hypoxemia. We clarify the difference between hypoxemia (low oxygen in the blood) and hypoxia (low oxygen at the tissue level), and walk through the major causes of hypoxemia that you need to recognize quickly at the bedside.

Key ConceptsHypoxemia vs. Hypoxia: Know the Difference Hypoxemia = Low oxygen in the blood. + Measured indirectly by SpO₂ (pulse oximeter) or directly by PaO₂ (arterial oxygen tension) or SaO₂ (oxygen saturation). * Hypoxia = Low oxygen at the tissue level. + Can happen with or without hypoxemia. Four Types of Hypoxia1. Hypoxemic Hypoxia: Blood oxygen is low, so tissues get less oxygen. (e.g., severe pneumonia) 2. Anemic Hypoxia: Low hemoglobin levels mean less oxygen-carrying capacity, even if oxygen levels are normal. (e.g., hemorrhage, hemolysis) 3. Ischemic Hypoxia: Blood flow to tissues is blocked or reduced. (e.g., MI, stroke, severe shock) 4. Histotoxic Hypoxia: Oxygen delivery is normal, but tissues can’t use it. (e.g., carbon monoxide or cyanide poisoning) Five Major Causes of Hypoxemia1. Hypopnea/Apnea (Decreased Respiratory Drive) * Inadequate breaths (or no breaths) means lower oxygen intake. * Seen in cardiac arrest, drug overdose, severe brain injury. * Easy to recognize as patients are encephalopathic or apneic. 2. High Altitude * Lower barometric pressure = less available oxygen, despite 21% FiO₂. * Rarely relevant inside hospitals, but important to know. 3. Diffusion Defect * Impaired oxygen transfer across alveoli, often due to chronic lung disease. * Examples: interstitial lung disease, idiopathic pulmonary fibrosis. * Patients are usually known to have underlying disease. 4. V/Q Mismatch (Dead Space Disease) * Problem with perfusion relative to ventilation * Common examples: + Pulmonary embolism (classic dead space). * Other causes include: + Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow. + Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli. + Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but unperfused areas. + Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation. * Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch. * Key point: Patients often oxygenate “ok” at rest but are tachypneic 5. Shunt (Most Common and Most Concerning) * “Crap in the alveoli” blocks oxygen diffusion: + Pneumonia (pus) + Pulmonary edema (water) + Atelectasis (collapse) + Pulmonary hemorrhage (blood) * Blood moves from right to left without being oxygenated. * Refractory hypoxemia despite oxygen therapy = shunt physiology. * Key Move: High FiO₂ (non-rebreather mask) → if still hypoxemic, they need positive pressure (NIV or intubation). Practical Bedside Approach Give as much FiO₂ as possible (non-rebreather mask). * Watch SpO₂ response: + If it improves → V/Q mismatch or dead space more likely. + If it doesn’t improve → think shunt physiology. * If refractory hypoxemia persists → Start positive pressure ventilation (HFNC, CPAP, BiPAP, or intubation depending on the situation). Clinical Bottom LineMastering the basics of hypoxemia helps you recognize dangerous physiology early — before your patient crashes. Keep in mind the four types of hypoxia and the five major causes of hypoxemia.

Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)

Guest Contributor###### Eric Acker

MDInternal Medicine Resident,Rising Chief Resident,Cape Fear Valley Medical Center,Fayetteville NC

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Ethical and LegalRead MoreShowing Slide 1 of 7The post REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) appeared first on REBEL EM - Emergency Medicine Blog.

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Acetaminophen (APAP) overdose remains one of the most common causes of acute liver failure in the United States. While its therapeutic use is widespread and generally safe, unintentional overdoses and delayed presentations can lead to devastating outcomes. In this episode of REBEL Cast, we break down the pathophysiology, clinical course, diagnostic approach, and evidence-based management of APAP toxicity—including when to initiate NAC, how to apply the Rumack-Matthew nomogram, and the evolving role of adjunctive therapies like fomepizole. Whether you’re in the ED or elsewhere , this is core content every clinician should know.

Click here for Direct Download of the Podcast.

Definition and Physiology

• After ingestion of a therapeutic dose, immediate release APAP is absorbed with a time to peak concentration anywhere between 30-45 minutes. In the context of extended-release, formulations, full absorption is typically reached by 4 hours post-ingestion.1
• In therapeutic dosing, the vast majority of APAP undergoes hepatic conjugation with glucuronide or sulfate to form benign metabolites that ultimately get excreted in the urine. The remaining ~5% is oxidized by CYP2E1 to form N-acetyl-p-benzoquinoeimine (NAPQI). NAPQI is hepatotoxic. Glutathione combines with NAPQI to generate non-toxic metabolites that are also eliminated in the urine.
• In overdose, the amount of NAPQI that is generated is increased as the typical metabolic pathways become saturated. The NAPQI that remains leads to hepatocellular death in Zone 3 of the liver (or the centrilobular location) which is the area with the largest degree of oxidative metabolism.

Clinical Manifestations and Diagnostic Evaluation

• The clinical course of acute APAP toxicity is classically broken into four different stages.
  • Stage1: this is generally within 24 hours. Patients are either asymptomatic or have non-specific GI symptoms (nausea, vomiting, malaise). At this point, hepatic function testing is normal.
  • Stage2: ~24-72 hours. The onset of hepatic injury marks this stage. Aspartate aminotransferase (AST) is the most sensitive marker to detect hepatic dysfunction; AST elevated is nearly universal by 36 hours post-ingestion.
  • Stage3: defined as peak hepatotoxicity; generally between 72-96 hours post-ingestion. Patients may manifest hepatic encephalopathy or coma. AST and/or ALT might rise above 10,000 IU/L. Other lab abnormalities include: INR/PT, glucose, lactate, pH, and creatinine. Death from fulminant hepatic failure usually occurs anywhere between 3-5 days after an acute ingestion. Mortality is often secondary to multiorgan failure, ARDS, sepsis, or cerebral edema.
  • Stage4: often called the “recovery phase.” Patient who survive demonstrate complete hepatic generation without any evidence of hepatic dysfunction.
• The following labs should be obtained for severe APAP ingestions:
  • APAP Concentration, hepatic panel, pH, coagulation panel, renal function, lactate and phosphate. These labs will ultimately dictate disposition (see King’s College Criteria below)

Management

• Consider GI decontamination with activated charcoal as this can reduce systemic absorption and limit subsequent clinical sequalae.
• Ingestions should be classified as acute or repeated supratherapeutic (“chronic” ingestions)
  • Single Acute Ingestion
    • If feasible, obtain a 4 hour post-ingestion APAP concentration. Any concentration earlier than 4 hours is uninterpretable as subsequent concentrations may increase or decrease depending on the clinical scenario.
    • Concentrations between 4-8 hour post-ingestion can be plotted on the Rumack-Matthew nomogram to determine when NAC should be initiated.
    • If the APAP concentration is above the plotted line, NAC should be started.
      • NAC is nearly 100% effective if started within 8 hours post-ingestion.2
    • If an APAP concentration is unable to be drawn before 8 hours or if LFTs are already elevated, NAC should be empirically started if the pre-test probability is high enough for clinical concern.
  • Repeated Supratherapeutic/Chronic Ingestions
    • Cannot apply the Rumack-Matthew Nomogram
    • If LFTs are elevated or if there is a positive APAP concentration, NAC should generally be started however consultation with a toxicologist or Poison Control Center is advised as these cases are often complicated.
• N-Acetyl-Cysteine (NAC) Dosing
  • “3 Bag Protocol” – 21 hour regimen
    • 150mg/kg over 1 hour loading dose
    • 50mg/kg over 4 hours = 12.5 mg/kg/hr
    • 100mg/kg over 16 hours = 6.25 mg/kg/hr
  • Risk: anaphylactoid reaction
    • Reaction is rate related and typically occurs during the loading dose
    • Symptoms: flushing, urticaria.
  • NAC should be continued until all of the following criteria are met:
    • Negative APAP concentration
    • “Significant Decreased in AST”: defined as either <1000 IU/L or a 25-50% drop from the peak.
    • No evidence of hepatic failure
  • If criteria are not met, the third bag should be extended indefinitely.
• The King’s College Criteria should be used as this set of lab work is used to determine which patients should be referred for possible liver transplant evaluation.3, 4
  • Arterial pH < 7.30
  • INR > 6.5 (PT >100 sec)
  • Creatinine > 3.4
  • Grade III or IV hepatic encephalopathy
  • Hyperlactatemia
  • Hyperphosphatemia
• Fomepizole (traditionally used for the treatment of toxic alcohols) has been used as an adjunctive treatment for massive acetaminophen toxicity as it has demonstrated efficacy in mitigating serum transaminase elevation, hepatic necrosis, and oxidative stress in both mouse and human models.5-8
  • As large scale human studies have yet to be published, fomepizole should NOT be routinely administered for APAP toxicity.

Take Home Points

1. Acetaminophen (APAP), most commonly referred to as “Tylenol” in the United States, is in a variety of pharmaceuticals. Medications like Excedrin, Fioricet, Percocet, Vicodin, and Day/Nyquil all contain acetaminophen.
2. Given the lack of a toxidrome, there should be a low threshold to obtain a screening acetaminophen concentration in the undifferentiated poisoned patient.
3. In overdose, acetaminophen leads to generation of NAPQI which is hepatotoxic. N-Acetylcysteine (NAC) is the antidote of choice and ideally should be administered within 8 hours of an acute ingestion.
4. To determine which patients should be treated with antidotal therapy, the Rumack-Matthew Nomogram should be utilized. Of note, this nomogram was validated for a single concentration obtained at or greater than 4 hours after a single, acute ingestion. (i.e. patients with repeated ingestions cannot be applied to the nomogram).
5. In patients with a high pre-test probability of APAP poisoning, the King’s College Criteria should be considered; this is a set of lab markers that help determine when patients should be immediately referred for liver transplant.
6. While physiologic plausibility exists for the use of fomepizole to treat severe APAP toxicity, no large scale human studies exist at this time to suggest that it should be routinely given for toxicity. As with all cases of toxicity, please call your local poison control center for assistance.

References

1. Hendrickson RG, McKeown NJ. Chapter 33. Acetaminophen. In: Nelson LS, et al., editors. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019.
2. Smilkstein MJ, Knapp GL, Kulig KW, Rumack BH. Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose: Analysis of the National Multicenter Study (1976 to 1985). N Engl J Med. 1988;319(24):1557-1562. PMID: 3059186
3. O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97(2):439-445. PMID: 2490426
4. King’s College Criteria for Acetaminophen Toxicity. Available at: https://www.mdcalc.com/calc/532/kings-college-criteria-acetaminophen-toxicity#next-steps
5. Akakpo JY, Ramachandran A, Duan L, et al. Delayed treatment with 4-methylpyrazole protects against acetaminophen hepatotoxicity in mice by inhibition of c-jun N-terminal kinase. Toxicol Sci. 2019;170(1):57-68. PMID: 30903181
6. Akakpo JY, Ramachandran A, Kandel SE, et al. 4-Methylpyrazole protects against acetaminophen hepatotoxicity in mice and in primary human hepatocytes. Hum Exp Toxicol. 2018;37(12):1310-1322. PMID: 29739258
7. Shah KR, Beuhler MC. Fomepizole as an adjunctive treatment in severe acetaminophen toxicity. Am J Emerg Med.2020;38(2):410.e5-410.e6. PMID: 31785979
8. Kang AM, Padilla-Jones A, Fisher ES, et al. The effect of 4-methylpyrazole on oxidative metabolism of acetaminophen in human volunteers. J Med Toxicol. 2020;16(2):169-176. PMID: 31768936

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Introduction: In this episode of Rebel Cast, host Marco Propersi, along with co-hosts Steve Hochman and Kim Baldino, delve into the practice and importance of street medicine—the direct delivery of healthcare to homeless and unsheltered individuals. Special guests Dr. Jim O’Connell, a pioneer of street medicine, and Dr. Ed Egan, a recent street medicine fellowship graduate, share their experiences and insights on serving this vulnerable population. They discuss the origins, scope, and challenges of street medicine, the ethical dilemmas faced, and the profound impact of building trust and community with patients. The conversation underscores the necessity of integrating street medicine with mainstream healthcare systems and emphasizes that small acts of kindness and persistence can significantly improve the lives of those experiencing homelessness.REBEL Cast – Street Medicine: Compassionate Care for the UnhousedClick here for Direct Download of the Podcast.

• 00:00 Introduction to Rebel Cast
• 00:18 Meet the Hosts and Guests
• 00:47 Understanding Street Medicine
• 02:22 Origins and Early Challenges
• 07:23 Street Medicine in Practice
• 20:11 Barriers to Care
• 22:23 Housing First Experiment
• 26:56 Ethical Dilemmas in Street Medicine
• 27:52 Challenges of Providing Care on the Streets
• 29:56 The Role of Street Medicine Teams
• 31:17 The Importance of Building Trust
• 33:55 Limitations and Realities of Street Medicine
• 37:37 The Future of Street Medicine
• 41:42 Integrating Street Medicine with Emergency Medicine
• 43:36 Personal Reflections and Lessons Learned
• 48:56 Advice for Aspiring Street Medicine Practitioners
• 53:03 Final Thoughts and Encouragement Links:1. Street Medicine Institute
• National Healthcare for the Homeless CouncilEMRA Fellowship Guide: Opportunities for Emergency Physicians, 3rd ed.

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Take Home points:

• Always suspect an open joint if there is a laceration, regardless of size, the lies over joint
• CT scan of the affected joint is widely considered to be the standard approach to evaluation but the saline load test may be useful in certain circumstances.
• Obtain emergency orthopedics consultation for all open joints and administer antibiotics and update tetanus in all patients

REBEL Core Cast 131.0 – Traumatic ArthrotomyClick here for Direct Download of the Podcast.

Definition: a deep laceration that extends into the joint capsule, exposing the intra-articular surface to the environment

• A laceration into the joint exposes the normally sterile intra-articular contents to external contamination
• Inoculation of the joint often results in septic arthritis

Physical Exam:

• Laceration over joint (can be variable in size)
• Local wound exploration may be sufficient in identifying the open joint
• Exam findings suspicious for joint capsule involvement:
  • • Air bubbles
    • Extravasation of joint fluid – straw colored, viscous, sometimes oily in appearance

Diagnostic testing:

• Imaging:
  • X-ray
    • Limited ability to see air in joints but a reasonable first test
  • CT scan
    • Intra-articular air visualized on CT (Konda 2013)
      • May be up to 100% sensitive for joint violation
      • Study limited by small numbers, inclusion bias + inadequate gold standard
    • May be considered the standard evaluation modality in many settings.
• Saline load test
  • Has mainly been supplanted by CT scan due to ease in obtaining, reported performance characteristics, consultant recommendation and difficulty in interpreting test.
  • Useful if physical examination equivocal or plain radiographs non-diagnostic
  • Technique (Video)
    • Perform arthrocentesis of the joint with a large bore needle (18-20 gauge)
    • Sterile saline is injected into the joint while passive movement is applied to the joint
    • The laceration site is watched for saline extravasation indicating communication between the joint and external environment
• • Sensitivity ranges from 34%-99% depending on the study, joint, and the amount of saline used to load the joint (Browning 2016)
  • Methylene blue
    • Aids in distinguishing a true positive from additional bleeding from the wound
    • Recent studies suggest that the addition of methylene blue does not increase sensitivity if a sufficient amount of saline is used (Metzger 2012)
  • Volume of fluid injected
    • Varies depending on the joint in which you are injecting
    • Higher volumes increase sensitivity but also increase pain for the patient
    • Knee Joint (Keese 2007)
      • 50 ml: Sensitivity of about 46%
      • 194 ml: sensitivity of 95%
    • Elbow Joint (Feathers 2011)
      • 20 ml: Sensitivity of 86%
      • 40 ml: Sensitivity of 95%
    • Ankle Joint (Bariteau 2013)
      • 7 ml: Sensitivity of 50%
      • 30 ml: Sensitivity of 95%

ED Management:

• Reduce open fractures if present
• Irrigate grossly contaminated wounds in the ED
• Immobilize the joint to prevent further injury
• Obtain early orthopedic evaluation for joint exploration, and washout to be performed within 6-24 hours
• Tetanus prophylaxis
• Prophylactic antibiotics (best if given within 6 hours)
  • Staph/strep coverage: 1st generation cephalosporin (i.e. cefazolin or cefuroxime)
  • If risk factors for MRSA present, use agent with activity against MRSA (i.e. vancomycin)
  • If significant soft tissue injury, add gram negative coverage like late generation cephalosporin, extended-spectrum penicillin, or aminoglycoside (i.e. gentamycin)
  • If concern for fecal or clostridial infection, add high dose penicillin (i.e. zosyn)
  • If seawater contamination and concern for vibrio vulnificus, add doxycycline

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Take Home Points

1. Early diagnosis: erythema and warmth of the skin surrounding the umbilicus isn’t normal. Get labs, start abx and get the patient admitted
2. Consult peds surgery on all of these patients as progression to nec fast, while uncommon, is devastating
3. If the patient appears toxic or has systemic symptoms, the simply omphalitis has progressed and aggressive treatment including surgery is likely indicated

REBEL Core Cast 130.0 – OmphalitisClick here for Direct Download of the Podcast.

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Take Home Points

1. Orogastric lavage may still play an important role in treatment of the overdose patient. Do not perform lavage if the ingestion has limited toxicity at any dose or the ingested dose is unlikely to cause significant toxicity.
2. Strongly consider orogastric lavage in a patient who has taken an overdose of drugs that are particularly toxic, suspected extreme doses associated with high morbidity/mortality and do not have easily available and effective antidotes.
3. Secure the airway prior to placing the lavage tube to minimize aspiration risk.

REBEL Core Cast 129.0 – Gastric LavageClick here for Direct Download of the Podcast.

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Take Home Points

1. Toxic alcohols generally refer to methanol and ethylene glycol as these substances pose significant metabolic derangement and end-organ damage.
2. Patient who present shortly after ingestion will simply look inebriated – no different than ethanol intoxication. At this point, patients will have an elevated osmolar gap and little to no anion gap.
3. Patient who presents in a delayed fashion after ingestion may have a normal osmolar gap however will manifest the signs of end-organ damage: anion gap metabolic acidosis, visual impairment, or renal dysfunction.
4. The osmolar gap is poorly sensitive, specific surrogate measure that is used to detect the presence of toxic alcohols. A normal osm gap does not rule out a toxic alcohol ingestion.
5. Management includes fomepizole, hemodialysis, and vitamin supplementation.

REBEL Core Cast 128.0 – Toxic AlcoholsClick here for Direct Download of the Podcast.

Reference: Wiener SW. Chapter 106. Toxic Alcohols. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, , Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 11e New York, NY: McGraw-Hill; 2019. Accessed October 2, 2024.

Guest Expert: Dr. Sanjay Mohan, MD (Link)

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Take Home Points

• Anticipate anatomically challenging airways and consider early intubation prior to loss of airway anatomy.
• Skip the zones of the neck and focus on hard signs of vascular (Shock w/o another source, Pulsatile bleeding, Expanding hematoma, Audible bruit, Signs of stroke) or aerodigestive (Airway compromise, Bubbling wound, Extensive SubQ air, Stridor, Significant hemoptysis/hematemesis). The presence of hard signs indicates the need to go to the OR or for angiographic intervention.
• Control hemorrhage with a single finger and direct pressure.

REBEL Core Cast 127.0 – Penetrating Neck InjuriesClick here for Direct Download of the Podcast.

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Take Home Points

• Early administration of antibiotics (within 60 min) in patients with fever and neutropenia is life saving.
• Fever in sickle cell is an emergency and always requires cultures and antibiotics even if the child appears well.
• Avoid sedation and lying supine and steroids in patients with mediastinal masses.
• Red flags in patients with headaches that may suggest a brain tumor include signs of increased intracranial pressure, focal neurological signs, seizures or ataxia.

REBEL Core Cast 126.0 – Peds Hem Onc EmergenciesClick here for Direct Download of the Podcast.

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Take Home Points

• Always obtain an EKG in patients with ESRD upon presentation
• Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
• If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
• In patients who are anuric, early mobilization of dialysis resources is critical

REBEL Core Cast 125.0 – HyperkalemiaClick here for Direct Download of the Podcast.

Definition: A serum potassium level > 5.5 mmol/L

Epidemiology

• Common electrolyte disorder
• 10% of hospitalized patients (Elliott 2010)

Causes

• Pseudohyperkalemia: extravascular hemolysis
• Renal failure (potassium is primarily eliminated by the kidneys)
• Acidosis
• Massive cell death (tumor lysis syndrome, rhabdomyolysis, burns, crush injuries, hemolysis)
• Drugs: ACEI, ARBs, Spironalactone, NSAIDs, Succinycholine

Clinical Manifestations

• Mild hyperkalemia often asymptomatic
• Cardiac Effects
  • Increased potassium raises the resting membrane potential of cardiac myocytes
  • Slows ventricular conduction
  • Decreases length of action potential
  • Increases cardiac myocyte excitability
  • Cardiac effects can manifest in lethal dysrhythmias
• Neuromuscular Effects
  • Paresthesias
  • Weakness
  • Flaccid paralysis
  • Depressed or absent deep tendon reflexes

Diagnosis

• Suspect hyperkalemia in ALL patients with renal impairment, especially end-stage renal disease (ESRD)
• Serum potassium
  • Can be artificially elevated by extravascular hemolysis
  • Blood gas results may differ from standard metabolic panels by up to 0.5mmol/L
• 12-Lead EKG
  • Screening test that can rapidly detect severe cardiac manifestations of hyperkalemia
  • A normal EKG with a significant serum potassium elevation should raise concerns for spurious results (extravascular hemolysis)
  • Sensitivity of EKG to detect hyperkalemia is poor (Wrenn 1991, Aslam 2002, Montague 2008)
  • Classic EKG findings
    • PR prolongation
    • Peaked T waves
    • Loss of P waves
    • Widening of QRS complex
    • Sine wave
    • Ventricular Fibrillation
    • Asystole
  • Note: Hyperkalemia can present with a number of “non-classic” EKG findings including AV blocks and sinus bradycardia (Mattu 2000)
  • Note: Hyperkalemic EKG changes do not necessarily occur in order (i.e. patients can jump from peaked T waves to sine wave)

Management

Basics: ABCs, IV, O2, Cardiac Monitor and, 12-lead EKG

• Identify + treat underlying cause of hyperkalemia (i.e. rhabdomyolysis -> hydration)
• Remove inciting factors (i.e. stop ACEI, NSAIDs etc)

Asymptomatic Patients without EKG Changes

• Eliminate potassium from the body
  • Binding agents (SPS, Sodium zirconium cyclosilicate etc)
  • Enhance renal elimination
    • Intravenous hydration if volume depleted
    • Consider potassium wasting loop diuretics (i.e. furosemide)
  • Dialysis for anuric patients (i.e. ESRD)

Symptomatic Patients or Significant EKG Changes

• Stabilize cardiac myocytes with calcium salts
  • Mechanism: Recreates the electrical gradient leading to rapid reversal of cardiac effects and rapid stabilization
  • Two Options: CaGluconate, CaCl2
    • No difference in time to onset (1st pass metabolism is a myth)
    • Dose: 1 ampule CaCl2 (270 mg Ca2+) = 3 ampules CaGluconate (90 mg Ca2+/ampule)
  • Onset of action: seconds to minutes
  • Duration: 20-30 minutes
• Shift potassium into intracellular space (temporary)
  • Insulin (Moussavi 2021)
    • Mechanism: Activation of the Na-K-ATPase
    • Dose: 5-10 units IV
    • Onset of Action: < 15 min
    • Effect: Lowers potassium by about 0.6 mmol
    • Duration of action: 30-60 min
    • Give with dextrose (0.5 – 1 g/kg) unless hyperglycemia present
    • Caution: Duration of action of insulin may outlast administered dextrose. Be vigilant for hypoglycemia
  • Beta-adrenoreceptor agonists (i.e. albuterol)
    • Mechanism: Activation of beta receptors
    • Dose: 10-20 mg inhaled (4-8 standard ampules)
    • Onset of Action: < 15 min
    • Effect: Lowers potassium by about 0.6 mmol
    • Duration of action: 30-60 min
    • Additive effect with insulin (Allon 1990)
    • Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications
  • Sodium Bicarbonate (NaHCO3)
    • Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory (Elliott 2010, Weisberg 2008)
• Eliminate potassium from the body (see above)

Asymptomatic Patients with Minor EKG Changes

• Minimal recommendations on managing this clinical entity
• Eliminate potassium from the body (see above)
• Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection
• Consider medications to shift potassium intracellularly while waiting for elimination

Take Home Points

• Always obtain an EKG in patients with ESRD upon presentation
• Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
• If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
• In patients who are anuric, early mobilization of dialysis resources is critical

References

Elliott MJ et al. Management of patients with acute hyperkalemia. CMAJ 2010; 182(15): 1631-5. PMID: 20855477

Wrenn K et al. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 1991; 20(11): 1229-32. PMID: 1952310

Aslam S et al. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in hemodialysis patients. Nephrol Dial Transplant 2002; 17: 1639-42. PMID: 12198216

Montague BT et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324–330. PMID: 18235147

Mattu A et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000; 18: 721-9. PMID: 11043630

Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869–872. PMID: 2266671

Weisberg LS. Management of hyperkalemia. Crit Care Med 2008; 36: 3246-51. PMID: 18936701

Moussavi K et al. Reduced alternative insulin dosing in hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy 2021; 41(7): 598-607. PMID: 33993515

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Take Home Points

• Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed.
• Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement.
• If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered.

REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia TherapyClick here for Direct Download of the Podcast.

Background and Physiology

• Shock secondary to beta-blocker (BB) or calcium-channel blocker (CCB) toxicity bears a tremendous degree of morbidity and mortality.
• According to the 2022 Annual Report of the National Poison Data System from America’s Poison Center, CCBs and BBs account for the sixth and seventh largest number of fatalities from overdose.1
• Recall that cardiac output is a function of both stroke volume and heart rate. The natural response to diminishing stroke volume is a compensatory rise in heart rate (tachycardia). Keep a low threshold to search a patient’s medication list for BB/CCBs, when a hypotension is seen with a “normal heart rate.”

Clinical Manifestations

• Both BBs and CCBs ultimately cause reduced levels of intracellular calcium within myocytes. Depending on the degree of toxicity, subsequent effects include: decreased systemic vascular resistance, vasodilation, bradycardia, various conduction delays, and ultimately hypotension and cardiogenic shock.
• In addition to abnormal vital signs, look for surrogates of poor clinical perfusion: acidemia, lactate, decreasing urinary output

Traditional Management

• Consider GI decontamination to reduce systemic absorption: 1g/kg up to 50g of activated charcoal. Patient must be alert or the airway must be secured as to avoid aspiration.
• Obtain multiple lines of intravenous access (3 PIVs or triple lumen CVC) and provide a judicious amount of fluids. (more on this below)
• Pharmacotherapy
  • Calcium Gluconate: 1-3g intravenous
  • Glucagon: 3mg-5mg slow intravenous push. Rapid administration may induce nausea and emesis.
• Vasopressors as a bridge to…

HIET

• Mechanism of action is still not fully elucidated however several factors are implicated:
  • Insulin augments cardiac contractility by activating “reverse-mode” Na-Ca exchange and subsequently increasing calcium concentration in the sarcoplasmic reticulum. 2
  • At a resting physiologic state, the heart utilize free fatty acids as its primary energy course. Under stressed conditions, glucose is used instead. Insulin helps to facilitate glucose metabolism.
• HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr.
  • If glucose <250 mg/dL, administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV.
• Ask pharmacy to concentrate insulin from 1 unit/mL to 10 units/ml.
  • Patients often succumb to volume overload given pre-existing cardiac disease and the volume of medical resuscitation through their hospital stay.
• Once HIET is initiated, dextrose and potassium infusions should simultaneously be started to obviate hypoglycemia and hypokalemia
  • Dextrose: 0.5-1 g/kg/hr via D50/D20
  • Replete potassium to a minimum of 3.5mEq/L
  • A central venous catheter (often a triple lumen) is often needed to emergently replete potassium and provide D50/D20 safely (given its high osmolarity)
  • Serial monitoring of dextrose (q15-30 minutes) and potassium (q1 hour) is critical
• HIET has been demonstrated to improve perfusion without necessarily increasing SVR/MAP – while MAPs may not markedly increase dramatically in the short term, obtain serial blood gases, lactate, and track urinary output to track perfusion. 3

Hyperinsulinemia Euglycemia Therapy (HIET) for BB/CCB Toxicity

1. Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed.
2. Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement.
3. HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr.
4. HIET therapy requires simultaneous dextrose and potassium infusions as insulin will induce hypoglycemia and shift potassium intracellularly.
5. If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered.

References

1. Gummin DD, Mowry JB, Beuhler MC, et al. 2022 Annual Report of the National Poison Data System® (NPDS) from America’s Poison Centers®: 40th Annual Report. Clin Toxicol (Phila). 2023;61(10):717-939. doi:10.1080/15563650.2023.226898
2. von Lewinski D, Bruns S, Walther S, Kögler H, Pieske B. Insulin causes [Ca2+]i-dependent and [Ca2+]i-independent positive inotropic effects in failing human myocardium. Circulation. 2005;111(20):2588-2595. doi:10.1161/CIRCULATIONAHA.104.497461
3. Holger JS, Engebretsen KM, Fritzlar SJ, Patten LC, Harris CR, Flottemesch TJ. Insulin versus vasopressin and epinephrine to treat beta-blocker toxicity. Clin Toxicol (Phila). 2007;45(4):396-401. doi:10.1080/15563650701285412

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Take Home Points:

• Posterior epistaxis is a rare, life-threatning presentation.
• The key is in identifying and rapidly gaining control with a posterior pack or foley catheter.
• These patients often require surgical intervention so get ENT to the bedside and admit to a place with a higher level of monitoring.

REBEL Core Cast 123.0 – Posterior EpistaxisClick here for Direct Download of the Podcast.

Recognition

• Typically will have heavy bleeding both anteriorly and posterior into the oropharynx. These patients have a tough time because they’re continually trying to spit out or swallow blood
• Tachycardia is common and hypotension while not common isn’t unexpected. Very different from anterior epistaxis where VS usually unremarkable or maybe a bit of hypertension
• Failure of anterior pressure or packing to stop bleeding: apply pressure but still see brisk posterior bleeding or even place b/l pack and see continued posterior bleeding

Start with the basics

• IV, Supp O2, Monitor
• Consider blood products if the patient appears to be losing a lot of blood or they report heavy blood loss. VS abnormalities can drive this as well
• Strongly consider reversal of AC (this will typically come after control)

Stopping the Bleeding

• PPE: these things bleed like stink. Anecdote. Gown, gloves and most importantly eye and face protection
• Ideal: commercial posterior pack
  • Two balloons – one for anterior, one for posterior
  • Place the device (straight back parallel to the floor)
  • Inflate anterior balloon (10-15 cc) of air
  • If still bleeding, inflate posterior balloon (5-10 cc of air)
• Foley: if no commercial device
  • Place foley catheter just as you would place a nasal tampon
  • When you see the tip of the foley in the posterior pharynx, inflate balloon (5-10 cc)
  • Need to pull back a bit and secure (can do this with tape on the nose)

Post Placement Care

• Antibiotics: standard practice to give cephalexin or amox/clav. Literature doesn’t defend this approach but, the lit is pretty sparse. The idea behind abx is to prevent things like AOM and TSS but neither should be much of an issue with short term placement
• ICU Admission?
  • Traditional teaching is that these patients are at risk for life-threatening bradydysrhythmias and should go to the ICU
  • Literature here is non-existent. Two oft-cited articles
    • Cassisi Laryngoscope 1971 – no mention of cardiac events in the article but widely cited
    • Zeyyan Laryngoscope 2010 – slightly lower HR in the packing group but no bradydysrhythmias
  • Before throwing ICU out
    • Hypoxia can occur – Cassisi found about a 20 mm Hg drop in PaO2 but all the patients in this publication were sedated so the packing may not have been the issue
    • look at Viducich 1995 Acad Emerg Med – showed that 18% of the 88 patients with posterior epistaxis required a surgical intervention. With that in mind, you want to consider placing patients into a setting where they can be frequently reassessed – perhaps SDU. This will be pretty location specific. If you treat a posterior bleed at a hospital without ENT, I would transfer as surgical intervention is pretty common

REBEL EM: Do Patients with Epistaxis Managed by Nasal Packing Require Prophylactic Antibiotics?

REBEL EM: Do Patients with Posterior Epistaxis Managed by Posterior Packs Require ICU Admission?

EMRAP HD: Epistaxis Posterior Pack

References

1. Cassisi NJ et al. Changes in arterial oxygen tension and pulmonary mechanics with the use of posterior packing in epistaxis: a preliminary report. Laryngoscope 1971; 81(8): 1261-6. PMID: 5569677
2. Zeyyan E et al. The effects on cardiac function and arterial blood gas of totally occluding nasal packs and nasal packs with airway. Laryngoscope 2010; 120: 2325-2330. PMID: 20938948
3. Loftus BC et al. Epistaxis, medical history and the nasopulmonary reflex: what is clinically relevant. Otolaryngol Head Neck Surg 1994; 110: 363-9. PMID: 8170679
4. Viducich RA et al. Posterior epistaxis: clinical features and acute complications. Acad Emerg Med 1995; 25(5): 592-6. PMID: 7741333
5. Corrales CE, Goode RL. Should patients with posterior nasal packing require ICU admission. Laryngoscope 2013; 123: 2928-9. PMID: 24114977

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Background: In May of 2018, Andexanet alfa gained accelerated approval by the FDA for the reversal direct oral anticoagulants (DOACs) despite a lack of robust evidence for use. The 2022 AHA/ASA guidelines give the drug a level 2A recommendation and recommend it over the use of 4F-PCC (Greenberg 2022). FDA approval alongside guideline endorsement has led to the drug seeing a remarkable growth in use without a single high-quality study to support its use. The available data reports good hemostatic control: a subjective measure that is highly biased by unblinding and selection bias. More importantly, there are no studies comparing andexanet alfa to 4F-PCC or even placebo looking at important, patient-centered outcomes.

REBEL Cast WEE – ANNEXA-1 – Andexanet Alfa Associated with Harm in DOAC ReversalClick here for Direct Download of the Podcast.

Article: Connolly SJ et al. Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage (ANNEXA-1). NEJM 2024; 390(19): 1745-55. PMID: 38749032

Clinical Question: Does the use of andexanet alfa in patients on DOACs with intracerebral hemorrhage improved hemostatic efficacy?

Population: Patients > 18 years of age on a factor Xa inhibitor (taken within 15 hours of randomization) with an acute intracerebral hemorrhage.

Outcomes:

• Primary: Hemostatic efficacy assessed at 12 hours after randomization. Hemostatic efficacy was defined as:
  • Excellent hemostatic efficacy: Change in hematoma volume < 20%
  • Good hemostatic efficacy: Change in hematoma volume < 35%
  • Increase in NIHSS < 7 points at 12 hours
  • No receipt of rescue therapies within 3-12 hours from randomization
  • No surgery to decompress the hematoma within 3-12 hours from randomization.
• Secondary: Percent change from baseline in anti-factor Xa activity during the first 2 hours from randomization
• Safety Endpoints (assessed at 30 days)
  • Thrombotic events (ischemic stroke, myocardial infarction, VTE).
  • Death

Intervention: Andexanet alfa high-dose or low-dose bolus followed by infusion depending on time and dose from last DOAC use.

Control: Usual care

Design: Non-blinded, randomized controlled trial performed at 131 centers across 23 countries over 4 years.

Exclusions

• GCS < 7 at the time of consent
• NIHSS > 35
• Surgery planned within 12 hours of enrollment
• Thrombotic event within 2 weeks of enrollment
• Time from symptom onset > 6 hours
• Pregnancy

Results:

• Primary results
  • 581 patients were assessed for eligibility across 131 sites over 4 years
    • 31 excluded prior to randomization
    • 20 excluded after randomization due to consent issues
  • 530 analyzed for the safety outcomes
    • 263 patients assigned to andexanet alfa arm
    • 267 patients assigned to usual care arm
  • 452 patients were analyzed for the primary outcome
  • 85.5% (195/228) patients in the usual care arm received 4F-PCC
  • 78.1% (175/224) patients in the andexanet arm received the low-dose regimen

Critical Results

| Andexanet alfa | Usual Care | Difference (95% CI) | P Value | | Primary Outcome | Hemostatic Efficacy | 67% (150/224) | 53.1% (121/228) | 13.4 (4.6 – 22.2) | 0.003 | | NIHSS change < 7 points | 87.9% (188/214) | 83.0% (181/218) | 4.6 (-2.0 – 11.2) | | Secondary Outcome | Anti-Factor Xa % Change | -94.5% (-96.6 – 88.9) | -26.9% (-54.2 – -9.5) | | Safety Outcome | Thrombotic Events | 10.3% | 5.6% | 4.6 (0.1 – 9.2) | 0.048 | | TIA | 0 | 0 | | Ischemic Stroke | 6.5% | 1.5% | | Myocardial Infarction | 4.2% | 1.5% | | DVT | 0.4% | 0.7% | | PE | 0.4% | 2.2% | | Arterial Embolism | 1.1% | 0.7% | | Death | 27.8% | 25.5% | 0.51 |

Strengths:

• This is the first randomized trial comparing andexanet alfa to standard care in this patient group.
• Multicenter, multinational study increasing applicability of findings.
• Outcome assessors were blinded to treatment arm.
• Hematoma measurements were made with a standard protocol and central site adjudication.
• 12 hour NIHSS assessments were performed by health care professionals who were unaware of group assignments

Limitations:

• Study funded, designed, and supervised by AstraZeneca Pharmaceuticals the maker of Andexanet alpha. Although, this does not refute the findings of this study, it should make readers skeptical.
• Clinicians were not blinded to the treatment arm patients were randomized to. This may introduce bias particularly in terms of subsequent treatments (treatments outside of reversal are not detailed in the study).
• Primary endpoint is not patient centered.
• Convenience sample of patients which introduces bias.
• There are some baseline differences between groups and it’s hard to say how this may have influenced the results.
• Exclusion criteria are likely to be difficult for clinicians to assess real time leading to protocol violation (particularly items like planned surgery and recent thrombotic event).
• Dose adjustment for time from ingestion likely to lead to protocol violation as this info difficult to assess.
• Exclusion criteria: Removed the sickest patients.

Discussion:

• The positive primary and secondary outcomes
  • Both the primary (hematoma expansion) and secondary (anti-factor Xa reduction) outcomes were better in the andexanet group.
  • Unfortunately, these are disease-oriented outcomes instead of patient centered outcomes: the patient doesn’t care if their hematoma expands by 20% or 25% or 30%. They care about clinically important outcomes like disability or death.
  • The authors note that in other studies, hematoma expansion has been associated with worse outcomes, but this was clearly not demonstrated in this study as 90d mRS and death were the same between groups.
  • Bottom line is that there wasn’t even a hint of improved clinical outcomes in the andexanet group.
• Safety outcomes favored the usual care group
  • In general, larger studies or registries of patients are required to determine safety of a treatment.
  • In this study, however, there is a clear signal for harm even with a small group of patients under ideal circumstances (ie enrolled within a study).
  • Though death was not statistically different, the raw numbers favor usual care.
  • Thrombotic events were clearly increased in the andexanet group.
  • Across a larger group of patients outside of the pristine setting of a study, it is likely that we would see an increase in thrombotic events and death.
• Only 85.5% of patients in the usual care group received 4F-PCC
  • Though there isn’t abundant evidence for the use of 4F-PCC in this setting, it does represent standard practice.
  • The authors do not report about the subgroup of patients who did not receive 4F-PCC and their outcomes.
    • If this data shows worse outcomes with no reversal treatment, it would suggest that usual care with 4F-PCC may be superior to andexanet alfa for clinical outcomes.
    • If this data shows improved outcomes with no reversal treatment, it would suggest that specific reversal agents aren’t necessary.
• There were multiple protocol changes during the study. Typically, protocols should not be changed while the study is enrolling patients. This is often done to try to steer the data towards benefit.
• Initial power calculation was for 900 patients to achieve a 90% power to detect and absolute difference of 10% points in terms of hemostatic efficacy but then made an addendum to the protocol to stop after 450 patients.
  • After this stop point, the safety and monitoring board recommended the trial be stopped.
  • Though the authors state they had no knowledge of the effect prior, there is no clear explanation given for this change and it raises the possibility that the trial was stopped prior to additional data showing harm was collected.
• Drug cost
  • Andexanet alfa costs between $30 – 50,000/treatment. This only takes into account drug costs (ie not monitoring, nursing costs etc).
  • 4F-PCC costs around $5-6,000/treatment.

Author Conclusion: “Among patients with intracerebral hemorrhage who were receiving factor Xa inhibitors, andexanet resulted in better control of hematoma expansion than usual care but was associated with thrombotic events, including ischemic stroke.”

Clinical Take Home Point: The authors conclusions are correct. However, they don’t properly stress the findings.

Treatment of patients with intracerebral hemorrhage on a DOAC with Anexanet alfa did not improve clinical outcomes when compared to usual care. Based on safety data, andexanet alfa resulted in increased harm to patients. Andexanet alfa should not be part of the standard treatment in this scenario based on the available evidence.

References:

1. Greenberg SM et al. 2022 Guidelines for the Management of Patients with Spontaneous Intracerebral Hemorrhage: A Guideline from the American Heart Association/American Stroke Association. Stroke 2022; 53(7). PMID: 35579034
2. Connolly SJ et al. Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage (ANNEXA-1). NEJM 2024; 390(19): 1745-55. PMID: 38749032

For More Thoughts on This Topic Checkout:

• REBEL EM: ANNEXA-4 – Andexanet Alfa and Factor Xa Inhibitors
• First10EM: Andexanet Alfa – More Garbage Science in the New England Journal of Medicine
• EM Lit of Note: Disutility, thy Name is ANEXXA-4

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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Take Home Points:

• There are many causes of neutropenia, chemotherapy being by far the most dangerous.
• Febrile neutropenia is a condition conveying high mortality. Early administration of antibiotics is the only factor known to reduce this mortality.
• For a patient with neutropenic fever, remember that the body’s own flora is the greatest danger. Isolate, but do not wait to initiate treatment.
• Check old blood cultures and obtain new cultures prior to starting treatment.
• Identify low risk patients and send them home with PO antibiotics and close oncology follow-up in conjunction with your oncologist.

REBEL Core Cast 122.0 – Neutropenic FeverClick here for Direct Download of the Podcast.

Neutropenia and Neutropenic Fever

Neutropenia: An absolute neutrophil count less than 500 cells/mm3 or less than 1000 cells/mm3 with a predicted decline to less than 500 cells/mm3

ANC = WBC x (neutrophil% + band%)

Mild: 1000 – 1500

Mod: 500 – 1000

Severe: 100 – 500

Profound: <100

Background

• Neutrophils directly combat infection and are important to coordinating the body’s overall immune response.
• The loss of these cells leads to immunosuppression as well as decreased responsiveness of the immune system as a whole
• Patients with neutropenia will not only get very sick very quickly, but also will have blunted immune response and may not localize signs of infection well
• Fever or malaise may be their only presenting symptoms.
• Patients with hematologic malignancies are at highest risk for suffering profound and prolonged neutropenia. Particularly high risk are those undergoing induction chemotherapy or stem cell transplant. Allogeneic stem cell grafting is higher risk than autologous.

Neutropenic Fever: Fever (one reading of 38.3C or sustained 38.0C) + ANC < 500 cells/mm3 or expected to fall to < 500 cells/mm3 within the next 48 hours

Common problem during chemotherapy:

• 10-50% of patients with solid malignancy and >80% of patients with hematologic malignancy will experience at least one episode of neutropenia (IDSA 2010, Klastersky 2004)
• Associated with high morality:
• ~90% without antibiotics (Perron 2014, Klastersky 2009)
• ~2-21% when treated with early antibiotics (Clarke 2011, Kruderer 2006)
• Higher mortality rates with co-morbidities and hematologic malignancies
• Time to antibiotic administration has been shown to directly impact mortality (Perron 2014, Rosa 2014, Marín 2015)

Causes of neutropenia (Gibson 2014):

• Overconsumption
• Sepsis
• Autoimmune disease (SLE, rheumatoid arthritis, etc)

Underproduction by bone marrow

• Malnutrition – alcoholism, anorexia, etc
• Myelodysplastic syndrome
• Post-viral: varicella, measles, rubella, influenza, hepatitis, Epstein-Barr virus, HIV
• Drug induced: clozapine, methimazole, sulfasalazine, bactrim, b-lactam antibiotics, NSAIDs, ticlopidine, cephalosporins, chemotherapy

Chemotherapy:

• Includes many drugs and drug regimens, all with the goal of killing rapidly dividing cells. Of note, this particularly affects:
• Cancer cells – this is the reason chemotherapy works as treatment
• Neutrophils – with a life cycle of only 1-6 days, their numbers are impacted dramatically by chemotherapy
• Mucosa – destruction of dividing cells thins mucosal barriers, putting these patients at high risk for mucositis and bacterial invasion
• This creates a dangerous situation where the body’s barriers against bacterial invasion are broken down and, thus, the ability to combat infection is severely blunted. Antibiotics are effectively the only thing standing between these patients and overwhelming sepsis.

Pathogens (Gudiol 2013):

The pathogens responsible for neutropenic fever have changed over time.

• Initially, Gram (-) organisms translocated from the gut caused majority of cases of neutropenic fever
• This changed in the 1990s. Gram(+) infections became more common due to more fluoroquinolone prophylaxis against Gram (-) organisms and due to more prevalent use of indwelling catheters for outpatient treatment
• Over the past decade, there has been a resurgence of Gram (-) organisms due to increasing antibiotic resistance, particularly multidrug resistant E coli and klebsiella
• Given the increasing rates of antibiotic resistance, antibiotic stewardship is becoming increasingly important
• In the ED, we can contribute to antibiotic stewardship by checking old cultures and obtaining new ones prior to initiation of antibiotics

ED Evaluation and Management:

Resuscitate if necessary

• Patients with neutropenic fever may rapidly progress to septic shock.
• Give appropriate fluids, vasopressors, and antibiotics.
• Antibiotics need to be given as quickly as possible if unstable

Perform a complete review of systems and physical exam looking for signs of focal infection

Basic Blood Work

• CBC, BMP, LFTs, bilirubin levels
• Blood cultures
• If indwelling catheter present: 1 set from each line of indwelling catheter + 1 peripheral set
• If no indwelling catheter present: 2x peripheral sets

Additional testing based on signs and symptoms:

• Respiratory symptoms
• CXR
• Sputum cultures
• Dysuria
• Urinalysis
• Urine culture
• Abdominal pain
• CT abdomen and pelvis
• If diarrhea present, consider C difficile PCR (if available)

Isolation

• Good hand hygiene is the most effective way to prevent these patients obtaining nosocomial infections
• Use standard barrier precautions
• Keep anyone with potentially communicable illness out of the patient’s room – visitors, other patients, or healthcare workers
• No plants in the treatment room or nurse’s station
• Any stem cell transplant patient should be in a private room. If they have an allogenic transplant, use a HEPA filter with >12 air exchanges per hour
• Isolation is important for neutropenic patients, but do not let waiting on an isolation room delay obtaining cultures and initiating antibiotics

Specific Pathologies

Mucositis

• Mucositis is a high risk feature indicative of bacterial invasion through thinned mucus membrane barriers.
• Signs and Symptoms
• oral pain, erythema, edema, or lesions
• sinus pain or pressure
• rectal pain or lesions, any swelling suggestive of perirectal abscess
• abdominal pain
• Inspect the rectum for swelling possibly indicative of perirectal abscess.
• Digital rectal exam is generally discouraged due to concern of inducing bacteremia if mucus membranes are damaged in the process

Neutropenic Enterocolitis (Typhlitis):

• A feared complication of neutropenic fever is direct bacterial invasion of the intestinal mucosa causing necrotizing infection
• Most commonly at the ileocecal junction
• It presents with classic triad of neutropenia, fever, and RLQ pain. Mortality approaches 50% when present (Gorschlüter 2005)
• Surgery is avoided unless the bowel perforates, as these patients have poor wound healing and high surgical complication rates

Determine whether the patient is high or low risk:

High Risk Factors:

• HD instability
• Hematologic malignancy
• Uncontrolled or widespread malignancy
• Induction chemotherapy / hematopoietic stem cell transplant
• ANC <100

• 7 days of ANC <500

• Medical comorbidities (particularly COPD, cardiac disease, or diabetes)

Low Risk Factors:

• HD stable
• Solid tumor malignancy
• ANC >500
• Neutropenia expected to last <7 days
• No comorbidities

MASCC and CISNE risk calculators:

MASCC Score

Low risk = 21-26

High risk = <21

The MASCC Score will identify more patients as low risk, but will have more treatment failures / bounce-backs than the CISNE score (Ahn 2017, Coyne 2016)

CISNE Score

Low risk = 0

Intermediate risk = 1-2

High risk = 3-8

The CISNE score will identify fewer patients as low risk, but will result in fewer treatment failures/bounce-backs than the MASCC score (Ahn 2017, Coyne 2016).

Default to using whichever score your oncologist is more comfortable with.

Antibiotic Selection

• Check old cultures for prior infections and sensitivities (if available).
• Follow your hospital’s protocol (if available). This will have been formulated based on local resistance patterns and likely with input from your institution’s oncologists.
• High Risk Patients will need hospitalization and IV antibiotics.

General approach for IV antibiotic therapy:

• Begin with single broad spectrum agent which includes pseudomonas coverage such as cefepime, piperocillin-tazobactam, or a carbepenem
• Penicillin allergies other than anaphylaxis are not considered a contraindication to the use of cephalosporins such as cefepime
• If patient has anaphylactic reaction to penicillins, consider broad coverage with ciprofloxacin plus clindamycin or aztreonam plus vancomycin (IDSA 2010)
• Do not routinely start vancomycin. Add vancomycin if there is clinical suspicion for Gram (+) infection
• Signs of mucositis or cellulitis
• Indwelling catheter present on arrival
• Prior MRSA infection
• Patient already on Gram (-) prophylaxis such as fluoroquinolone
• Consider adding additional agents for unstable patients, or patients in which antibiotic resistant organisms are suspected (patient has known colonization or patient population has high endemic rates).
• MRSA: vancomycin, linezolid, or daptomycin
• VRE: linezolid or daptomycin
• Extended spectrum beta lactamase (ESBL) producing organisms: carbapenem
• Carbapenemase producing organisms (such as klebsiella): polymixin-colistin or tigecycline
• If there is clinical suspicion for influenza (or positive PCR testing), treatment with oseltamivir is recommended
• Other antiviral and antifungal agents should NOT be started routinely.
• Only start antiviral or antifungal therapies if the patient has a known viral or fungal infection (ex: patient spikes a fever while already on antifungal treatment) or if they have a clinical picture strongly suggestive of viral or fungal etiology
• Antifungals are generally not initiated until a patient has had >4 days of fever unresponsive to antibiotic treatment with no clear source identified

Low risk

• If the patient has no high risk features, is found to be low risk on MASCC or CISNE scoring, and has good oncology follow-up, it may be preferable to discharge them home with 24hr oncology follow-up
• Send patients home ONLY after discussion with the patient’s oncologist and only if there are no high risk features present

Outpatient antibiotic choice:

• Ciprofloxacin plus amoxicillin-clavulanate is recommended by IDSA guidelines for oral empiric therapy (IDSA 2010)
• Levofloxacin or ciprofloxacin monotherapy, or ciprofloxacin plus clindamycin are less well studied but are commonly used
• Avoid fluoroquinolones if the patient is already on fluoroquinolone prophylaxis

Take Home Points:

• There are many causes of neutropenia, chemotherapy being by far the most dangerous.
• Febrile neutropenia is a condition conveying high mortality. Early administration of antibiotics is the only factor known to reduce this mortality.
• For a patient with neutropenic fever, remember that the body’s own flora is the greatest danger. Isolate, but do not wait to initiate treatment.
• Check old blood cultures and obtain new cultures prior to starting treatment.
• Identify low risk patients and send them home with PO antibiotics and close oncology follow-up in conjunction with your oncologist.

Read More:

• Infectious Disease Society of America 2010 Clinical Practice Guidelines
• Life in the Fast Lane: Febrile Neutropaenia
• Uptodate: overview of neutropenic fever syndromes
• EMRAP: Risk stratification of neutropenic fever
• MDCalc: MASCC Score
• MDCalc: CISNE Score

References:

1. Ahn S, Rice TW, Yeung SJ, Cooksley T. Comparison of the MASCC and CISNE scores for identifying low-risk neutropenic fever patients: analysis of data from three emergency departments of cancer centers in three continents. Support Care Cancer. 2018 May;26(5):1465-1470. doi: 10.1007/s00520-017-3985-0. Epub 2017 Nov 22.
2. Clarke, R. T., Warnick, J., Stretton, K., Littlewood, T. J., Improving the immediate management of neutropenic sepsis in the UK: Lessons from a national audit. British Journal of Haematology. 2011 Jun;153(6):773-9. doi: 10.1111/j.1365-2141.2011.08693.x. Epub 2011 Apr 22
3. Coyne CJ, Le V, Brennan JJ, Castillo EM, Shatsky RA, Ferran K, Brodine S, Vilke GM. Application of the MASCC and CISNE Risk-Stratification Scores to Identify Low-Risk Febrile Neutropenic Patients in the Emergency Department. Ann Emerg Med. 2017 Jun;69(6):755-764. doi: 10.1016/j.annemergmed.2016.11.007. Epub 2016 Dec 29.
4. Ellis M. Febrile Neutropenia. Annals of New York Academy of Sciences. 2008 Sep;1138:329-50. doi: 10.1196/annals.1414.035.
5. Freifeld, A. G., Bow, E. J., Sepkowitz, K. A., Boeckh, M. J., Ito, J. I., Mullen, C. A., Raad, II, et al., Clinical practice guideline for the use of antimicrobial agents in neutropenic patients with cancer: 2010 update by the infectious diseases society of america, Clinical Infectious Diseases, 2011, 52(4):e56-93.
6. Gibson C, Berliner N. How we evaluate and treat neutropenia in adults. Blood. 2014 Aug 21;124(8):1251-8; quiz 1378. doi: 10.1182/blood-2014-02-482612. Epub 2014 May 28.
7. Gorschlüter M, Mey U, Strehl J, et al. Neutropenic enterocolitis in adults: systematic analysis of evidence quality. Eur J Haematol 2005; 75:1.
8. Gudiol C, Bodro M, Simonetti A, et al. Changing aetiology, clinical features, antimicrobial resistance, and outcomes of bloodstream infection in neutropenic cancer patients. Clin Microbiol Infect 2013; 19:474
9. Klastersky J. The changing face of febrile neutropenia-from monotherapy to moulds to mucositis. Why empirical therapy? J Antimicrob Chemother. 2009;14(Suppl 1):i14–i15
10. Klastersky J. Management of fever in neutropenic patients with different risks of complications. Clin Infect Dis. 2004;39(Suppl. 1):S32–S37
11. Kuderer NM, Dale DC, Crawford J, Cosler LE, Lyman GH. Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients. Cancer. 2006 May 15;106(10):2258-66.
12. Marín M, Gudiol C, Ardanuy C, Garcia-Vidal C. Jimenez L, Domingo-Domenech E, Pérez FJ, Carratalà J. Factors influencing mortality in neutropenic patients with haematologic malignancies or solid tumours with bloodstream infection. Clinical Microbiology and Infection. Volume 21, Issue 6, June 2015, Pages 583-590
13. Perron T, Emara M, Ahmed S. Time to antibiotics and outcomes in cancer patients with febrile neutropenia. BMC Health Services Research. 2014;14:162. doi:10.1186/1472-6963-14-162.Radiologypics, P. B. (2014, November 10). Neutropenic Colitis (Typhlitis). Retrieved from https://radiologypics.com/2014/11/10/neutropenic-colitis-typhlitis/Rosa RG, and
14. Goldani LZ. Cohort Study of the Impact of Time to Antibiotic Administration on Mortality in Patients with Febrile Neutropenia. Antimicrob Agents Chemother. 2014 Jul; 58(7): 3799–3803. doi: 10.1128/AAC.02561-1

Stiff, PJ. Coding for Mucositis. From presentation at ICD-9-CM Coordination and Maintenance Committee Meeting. Loyola University Medical Center. Centers for Disease Control. September 30, 2005. Retreived from https://www.cdc.gov/nchs/ppt/icd9/att_mucositis_sep05.ppt

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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Background: The holy grail of outcomes in OHCA is survival with good neurologic outcome. The only interventions proven to increase this outcome are high quality CPR and defibrillation in shockable rhythms. Ventilation is also an important component of resuscitation in OHCA. Excess minute ventilation can adversely affect hemodynamics due to increased intrathoracic pressure (i.e. decreased venous return). Additionally, low CO2 levels from hyperventilation can lead to cerebral vasoconstriction which could lead to worsened secondary brain injury.

Most organizations recommend adults to be ventilated with tidal volumes of 500 to 600mL/breath during ongoing CPR. Large adult BVMs can have maximum tidal volumes of ≈1500mL and deliver about 750mL per one handed ventilation. Simulation studies have shown that health care professionals often provide minute ventilation well above these recommended ranges.

One of the recommendations from many experts to mitigate the perceived risk of large adult BVMs is using smaller adult BVMs. This change would result in decreasing the maximum volume from 1500 to 1000mL and an expected delivered tidal volume from 750 to 450mL/breath (much more inline with recommended ranges). However, evidence that this approach makes is difference is lacking.

REBEL Cast 126: Should We Not Be Recommending Small Adult BVMs in OHCA?Click here for Direct Download of the Podcast

Paper: Snyder BD et al. Association of Small Adult Ventilation Bags with Return of Spontaneous Circulation in Out of Hospital Cardiac Arrest. Resuscitation 2023. PMID: 37805062

Clinical Question: Is large adult BVM or small adult BVM associated with more ROSC in adult patients treated with advanced airway placement for nontraumatic OHCA?

What They Did:

• Retrospective, observational cohort analysis of prospectively obtained data from a single urban EMS system
• Evaluating adults treated with advanced airway placement for nontraumatic OHCA
• Jan 2015 to Dec 2021
• Changed from large adult BVMs to small adult BVMs in summer of 2017 (3 month crossover period was allowed and excluded from analysis)
• Used a Mercury medical CPR-2 small ventilation bag
• Compared rates of ROSC, ventilation rate, and mean end tidal carbon dioxide (ETCO2) by minute before and after small adult BVM implementation

Outcomes:

• Primary: ROSC at the end of EMS care (i.e. Arrival to ED or terminated efforts in the field)
• Secondary:
  • Ventilation rate
  • Mean end-tidal CO2 (ETCO2) during CPR

Inclusion:

• Adult patients with nontraumatic OHCA
• Treated with an advanced airway (i.e. Endotracheal intubation or iGel)

Exclusion:

• Age <18 years
• Received basic life support only
• Termination of resuscitation due to advanced directives
• ALS interventions prior to EMS arrival
• Insufficient capnography data
• Cricothyrotomy
• Advanced airway placed while patient had spontaneous circulation
• Airway was managed with BVM only
• Did not receive CPR while under EMS ALS care

Results:

• 1994 Patients included in analysis
  • 1331 (67%) treated with small adult BVM
  • 663 (33%) treated with large adult BVM
  • 21% had an initial shockable rhythm
• ROSC
  • Small Adult BVM: 33%
  • Large Adult BVM: 40%
  • uOR 0.74; 95% CI 0.61 to 0.90; P = 0.003
  • After adjustment for age, sex, witnessed arrest, bystander CPR, and initial rhythm this finding remained statistically significant (aOR 0.74; 95% CI 0.61 to 0.91)
• Ventilation rates did not differ between cohorts (≈12BPM)
• ETCO2
  • Small Adult BVM: 36.9 +/- 19.2mmHg
  • Large Adult BVM: 33.2 +/- 17.2mmHg
  • P <0.01

Strengths:

• Written records are compared to cardiac monitor files and audio recordings to adjudicate differences before integrating information into the registry
• Intubations confirmed with ETCO2
• Took into account the COVID-19 pandemic time period
• Also took into account the potential for trends over time by visualizing the incidence of ROSC by month over a seven year period and found no significant change in the slope before and after the implementation of the small adult BVM

Limitations:

• Only included patients that were intubated with an endotracheal tube or iGel (these results may not apply in patients without these devices)
• There were some confounding baseline differences (explained more in discussion)
• Unclear what other interventions were performed in terms of ACLS medications or what the specific causes of the cardiac arrest were from
• This was a before and after study not allowing for a control group. Before and after studies can introduce numerous biases particularly if other pieces of care changed between the two time periods. (Can also go in the discussion)
• The actual tidal volume delivered was not measured in this trial and therefore the delivered minute ventilation is unknown
• As this is a retrospective study, we can only show association, BUT NOT causation of the size of the adult BVM affecting ROSC outcomes

Discussion:

• There are some key BASELINE DIFFERENCES that could account for the results of this trial (i.e. confounders):
  • More patients in the small adult BVM cohort received bystander CPR (64% vs 59%). This would favor more ROSC in the small adult BVM cohort
  • Unwitnessed arrest was slightly greater in the large adult BVM cohort (58% vs 53%)…This would favor more ROSC in the small adult BVM cohort
  • Fewer patients in the small adult BVM cohort arrested in public (22% vs 27%…Unclear how this would impact ROSC
  • The interval from 911 call to start of CPR (10 vs 9min) and advanced airway placement (20 vs 18min) were longer in the small adult BVM cohort…Not sure 1 to 2min of difference would result in more ROSC in the large adult BVM cohort
  • Adherence to guideline recommended ventilation rates of 10 BPM was more common in the small adult BVM cohort (28.4% vs 31.2%)…This would favor more ROSC in the small adult BVM cohort
  • It would appear most things at baseline favored the small adult BVM cohort (Although the authors did account for most of these in adjusted analyses)
• The end of this trial took place during the COVID-19 PANDEMIC:
  • Anyone who took care of cardiac arrest patients during the COVID-19 pandemic knows that there were significant delays in care
  • According to the authors any cases of OHCA that occurred after the start of the pandemic (Feb 2020) were censored from the analysis and the results were evaluated again
  • When looking at cases of OHCA that occurred prior to Feb 2020 the small adult BVM cohort had a similarly lower odds of ROSC (OR 0.75; 95% CI 0.60 to 0.93; p = 0.008) as the entire time period this intervention was implemented
  • This remained the case even after adjusting for initial rhythm, age, sex, witnessed arrest and bystander CPR (aOR 0.76; 95% CI 0.61 to 0.95; p = 0.018)
• While I would imagine during a code most people are bagging faster than 10BPM, in this study 6 to 18 BPM were delivered in 82.5% of the measured ventilations. Is this a result of Hawthorne effect or the implementation of a metronome to guide chest compression and ventilation rates (implemented June of 2015) or simply a well trained EMS system? This addition would seem to favor the small adult BVM group
  • This EMS organization appears to be very high functioning with lots of training and education which may not be the standard at other agencies. The fact that the medics are providing a good RR and good TV throughout a 7-year period would suggest this and in doing so a simple change from a large adult BVM to a small adult BVM may have resulted in the association of lower ROSC whereas an agency that does not get as much training or high functioning may actually still be causing harm with the large adult BVM
• Finally, there was a higher ETCO2 in the small adult BVM cohort compared to the large adult BVM cohort. As ventilatory rate was essentially similar between groups, this most likely means a smaller tidal volume was delivered with each breath. This smaller tidal volume could have lead to physiologic changes that are potentially harmful:
  • Hypoventilation
  • Increased dead space fraction
  • Alveolar decruitment
  • Atelectasis causing shunt physiology

Author Conclusion: “Use of small adult bag during OHCA was associated with lower odds of ROSC at the end of EMS care. The effects on acid base status, hemodynamics, and delivered minute ventilation remain unclear and warrant additional study.”

Clinical Take Home Point: This is a really messy trial, with lots of methodological and confounding issues that make it difficult to interpret. It does show that when experts recommend an intervention it is important to study it. Until better evidence shows us differently it is probably best to stick with a large adult BVM but use one hand for bagging and maintain a rate of 10BPM.

References:

1. Snyder BD et al. Association of Small Adult Ventilation Bags with Return of Spontaneous Circulation in Out of Hospital Cardiac Arrest. Resuscitation 2023. PMID: 37805062

Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami)

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Take Home Points

• Acute rhinosinusitis is a clinical diagnosis
• The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics
• Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement.

REBEL Core Cast 121.0 – Acute SinusitisClick here for Direct Download of the Podcast.

Definition:

• Acute rhinosinusitis (ARS) – Symptoms for less than four weeks
• Subacute rhinosinusitis – Symptoms for 4 to 12 weeks
• Chronic rhinosinusitis – Symptoms persisting greater than 12 weeks
• Recurrent acute rhinosinusitis – Four or more episodes of ARS per year, with interim symptom resolution

Epidemiology: (Anon 2004)

• 20 million cases of sinusitis annually in the US, costing $3.5 billion/year
• Source of 1 in 5 antibiotic prescriptions for adults

Presentation:

• Sinusitis is most commonly diagnosed by clinical symptoms
• Common symptoms
  • Purulent nasal discharge
  • Nasal congestion
  • Facial pain or pressure, especially over a sinus or unilaterally
  • Anosmia
  • Hyposmia
  • Fever
  • Cough
  • Fatigue
  • Maxillary pain
  • Ear pressure or fullness.

Classification of Sinusitis:

●Acute viral rhinosinusitis (AVRS)

• ARS with viral etiology (i.e. rhinovirus, influenza, and parainfluenza)
• Most common form of ARS

●Uncomplicated acute bacterial rhinosinusitis (ABRS)

• ARS with a bacterial etiology without clinical evidence of extension outside the paranasal sinuses and nasal cavity
• Bacterial superinfection: 0.5-2% of all ARS

●Complicated acute bacterial rhinosinusitis

• ARS with bacterial etiology with clinical evidence of extension outside the paranasal sinuses and nasal cavity

Sinusitis: Viral vs. Bacterial:

• Color change in sputum does not determine whether infection is viral or bacterial
• Viral infections
  • Tend to begin resolution by 7-10 days
  • Rarely have associated fevers
  • If fever present, usually only in the first 48 hours.
• Guidelines for diagnosing ABRS are
  • Presence of URI/cold symptoms that
• • • • Don’t improve after 10 days * Worsen after 5-7 days of improvement - Severe symptoms including high fever, purulent discharge or facial pain for 3-4 days

The Data Behind Antibiotic Use

• • Clinically diagnosed acute sinusitis - * Multiple studies show the same cure rate at 7 days, but improved cure rate at 7-14 days for those who use antibiotics (Lemiengre 2012, Berg 1986, Gwaltney 1996) * Overall Treatment Effect NNT = 18 * Overall Harm NNH = 8 (mostly GI side effects) - Radiographically-diagnosed acute sinusitis (Ahovuo-Saloranta 2008) * Endpoint: clinical cure at 7-15 days * NNT = 15 * NNH = 8

IDSA Recommendations for Antibiotic Treatment (Chow 2012)

• Patients that should be treated
  • Persistent symptoms w/o improvement (> 10 days)
  • Severe symptoms (> 3-4 days)
  • Worsening (“double-sickening”) (> 3-4 days)
• Antimicrobials
  • 1st Line
    • Amoxicillin 875 mg PO BID X 5-7 days
    • Doxycycline 100 mg PO BID X 5-7 days
  • 2nd Line
    • Amoxicillin/Calvulanate 875/125 mg PO BID X 5-7 days
    • Levofloxacin 500 mg PO Q24 X 5 days

Bottom Line: Given the risk for adverse events associated with antibiotic use, the growing specter of resistance and the lack of significant differences in outcomes with antibiotic use, it is better to avoid antibiotics in most patients with ARS. Antibiotics should be considered in those with severe disease and in immunocompromised patients

Take Home Points

• Acute rhinosinusitis is a clinical diagnosis
• The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics
• Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement.

References

1. Anon JB et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004; 130(Suppl 1): 1-45. PMID: 14726904
2. Lemiengre MB et al. Antibiotics for Clinically Diagnosed Acute Rhinosinusitis in Adults. Cochrane Database Syst Rev 2012. PMID: 23076918
3. Berg O et al. Occurence of asymptomatic sinusitis in common cold and other acute ENT-infections. Rhinology 1986; 24(3): 223-5. PMID: 3775189
4. Gwaltney JM. Acute community-aquired sinusitis. Clin Infect Dis 1996; 23(6): 1209-23. PMID: 8953061
5. Ahovuo-Saloranta A et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev 2008. PMID: 18425861
6. Chow AW et al. IDSA Clinical practice guideline for acute bacterial rhino sinusitis in children and adults. Clin Infect Dis 2012; 54(8): e72-e112. PMID: 22438350

Read More

• The NNT.com: Antibiotics for Clinically Diagnosed Acute Sinusitis in Adults
• The NNT.com: Antibiotics for Radiologically-Diagnosed Acute Maxillary Sinusitis

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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Podcast Direct Download: Link

Release Date: April 16th, 2024

Show Notes

The Visible Voices Podcast

Dr. Glaucomflecken: Power of Ultrasound with Emergency Medicine Dr. Resa Lewiss

Adaira I Landry MD

Resa E Lewiss MD is a Professor of Emergency Medicine at the University of Alabama at Birmingham. A TEDMED speaker and TimesUp Healthcare founder, she’s an internationally renowned point-of-care ultrasound educator and champion for diverse, equitable, and inclusive workplaces. She attended college at Brown, medical school at Penn, Emergency Medicine residency at Harvard, and fellowship at Mount Sinai St. Luke’s Roosevelt. She led point-of-care ultrasound sections at St. Luke’s Roosevelt, the University of Colorado, and Thomas Jefferson. A physician healthcare design consultant for Perkins&Will, her design focus has been ultrasound hardware and workflows. She’s helped to redesign the built environment of a Harvard ICU and an infectious diseases unit in Malawi. As host and founder of the Visible Voices Podcast, she’s interviewed dozens of subject matter experts in healthcare, equity, and current trends. Her writings are published in the popular press and scientific journals, such as Harvard Business Review, Slate, Nature, and Fast Company. Her new book, MicroSkills : Small Actions, Big Impact is forthcoming from HarperCollins in 2024.

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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REBEL Cast – EMTALA + Reproductive HealthClick here for Direct Download of the Podcast.

Dr. Dara Kass is a practicing emergency medicine physician who was most recently as the Regional Director of Region 2 for the US Department of Health and Human Services.

She currently works with organizations and institutions to advance and implement policies that affect the care of individuals in this new healthcare landscape, most specially related to all forms of reproductive health care from contraception and pregnancy termination to addressing the maternal mortality crisis in the United States.. Doctor Kass’s impact is broad as a tireless advocate, spearheading initiatives, and campaigns formatting improvements on issues such as gender equity, reproductive healthcare, and organ donation. Doctor Kass lives in Scarsdale NY with her husband and three children.

Dr. Monica Saxena is a practicing emergency physician and assistant professor at Stanford University School of Medicine.

Her research focuses on reproductive justice and women’s health in the emergency department setting. Dr. Saxena is the 2022 recipient of the Rising Star Faculty Award from the American College of Emergency Physicians. She holds a law degree from the University of Michigan and a medical degree from Wayne State University School of Medicine.

MedPage Today: The Ethos of Emergency Medicine Hangs in the Balance

Resources:

Reproductiverights.gov

Submit your complaint to the State Survey Agency in the state where the hospital is located.

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Background: The mainstay of treatment for symptomatic pulmonary embolism (PE) is anticoagulation (AC). Patients with higher-risk PE may require advanced interventions such as thrombolytic therapy, surgical thrombectomy, or even extracorporeal membrane oxygenation (ECMO). Because of its short half-life and availability of a reversal agent, unfractionated heparin (UFH) is commonly used when percutaneous or surgical interventions are being considered.

The standard weight based dosing of UFH is 80U/kg bolus followed by an infusion started at 18U/kg/hr, titrated to a target activated partial thromboplastin time (aPTT) of 1.5 to 2.5x the control range or an anti-Xa level of 0.3 to 0.7u/mL. The efficacy of UFH in reaching and maintaining appropriate anticoagulation is poorly understood.

REBEL Cast 125: 1st 48 Hours of PE Management – How Good is Unfractionated Heparin?Click here for Direct Download of the Podcast

Paper: Prucnal CK et al. Analysis of Partial Thromboplastin Times in Patients With Pulmonary Embolism During the First 48 Hours of Anticoagulation With Unfractionated Heparin. Acad Emerg Med 2020. PMID: 31625654

Clinical Question: How effective is UFH in obtaining appropriate anticoagulation during the first 48 hours of administration to patients with acute PE?

What They Did:

• Retrospective analysis of a PE response team (PERT) data base
• Single, large, urban academic teaching hospital (Massachusetts General Hospital)
• October 2012 to April 2017
• 2 Standard Dosing Regimens Evaluated
  • Bolus + Drip (Low Risk of Bleeding): 80U/kg + Continuous titrated infusion starting at 18U/kg/hr
  • Drip Only (Higher Risk of Bleeding): Continuous titrated infusion starting at 18U/hr
• Subsequent aPTT (seconds) and Rate Changes
  • <40: +3U/kg/hr
  • 40 – 49.9: +2U/kg/hr
  • 50 – 49.9 +1U/kg/hr
  • 60 to 80: No change
  • 1 to 100: -2U/kg/hr

  • 100: Hold for 60minutes then -3U/kg/hr

Outcomes:

• Proportion of patients with a therapeutic aPTT value during each 6 hour time period
  • A therapeutic aPTT was defined as a value of 60 to 80seconds
  • A therapeutic Anti-Xa level was defined as a value of 0.3 to 0.7u/mL

Inclusion:

• Adult patients
• Acute PE
• PERT team consulted
• Received anticoagulation with UFH according to guideline standard dosing

Exclusion:

• Patients treated with nonstandard dosing regimens

Results:

• 505 patients met inclusion criteria

  • PE Severity
    • Saddle: 17.4%
    • Rt Heart Strain on CT: 46.9%
    • Hemodynamic Collapse: 7.9%
    • Massive PE: 28.3%
    • Right Heart Strain on Echo: 21.4%
    • Elevated Troponin Level: 55.3%
  • Interventions Received:
    • Systemic thrombolysis: 4.0%
    • Catheter-Based Intervention: 5.9%
    • Surgical Thrombectomy: 2.0%
    • ECMO: 1.4%
    • IVC Filter: 5.0%
  • 30d Outcome:
    • Mortality: 5.7%
    • Re-Thrombosis: 3.9%
    • Bleeding: 3.0%
  • Therapeutic aPTT in patients receiving bolus and infusion of UFH
    • At 6hrs: 13.9% (10.2 to 18.5%)
    • At 12hrs: 19% (14.2 to 25.0%)
    • At 24hrs: 26.3% (25.3 to 33.1%)
    • At 36hrs: 28.3% (22.0 to 35.4%)
    • At 48hrs: 28.4% (20.8 to 37.5%)

• Therapeutic aPTT in patients receiving infusion only of UFH

  • At 6hrs: 14.5% (9.5 to 21.5%)
  • At 12hrs: 23.3% (15.2 to 32.3%)
  • At 24hrs: 41.4% (31.6 to 51.9%)
  • At 36hrs: 37.0% (26.8 to 48.5%)
  • At 48hrs: 42.1% (30.2 to 55.0%)

• No patients had all therapeutic aPTT values

Strengths:

• Asks a clinically important question
• Study was stratified for patients being treated with bolus plus titrated infusion or titrated infusion only
• Used UFH standard dosing strategies used by most physicians
• Performed a sensitivity analysis that excluded all patients treated with systemic or catheter-directed thrombolysis, surgical embolectomy, or ECMO

Limitations:

• Initiation of AC was defined as the order start time for UFH in the electronic medical record. There could have been delays in actually starting the UFH
• No real details on chart extraction methodology (i.e. how they handled incomplete or conflicting data)
• Only one abstractor where there is no assessment of the abstractors performance or comparison to another abstractor
• Unclear why one strategy was chosen over another
• Selection bias: Only patients consulted by PERT
• For patients with more than one aPTT value in a given 6 hour time period, the first therapeutic value was selected for analysis. If there was no therapeutic value, the first aPTT value reported was used
• Single center study meaning local factors may limit generalizability to other institutions
• Time outside therapeutic aPTT is not all equal. An aPTT that is slightly above or below the reference range would be considered outside the range (i.e. values close to the therapeutic cutoff were considered equivalent to those far from the cut-off range)
• This study does not determine whether time spent in the therapeutic range affects morbidity and mortality (Very low mortality rate = 6%)

Discussion:

• Only a minority of patients in whom the PERT team was consulted treated with UFH using standard dosing had a therapeutic aPTT during the first 48 hours of anticoagulation with the majority of patients being subtherapeutic
  • The proportion of patients in therapeutic range was lowest at 6 hours (14%) and highest at 42 hours (35%)
  • Approximately 40% of patients failed to reach the therapeutic range in the first 48 hours of AC
  • It wasn’t until 36 hours after the initiation of UFH that >50% of patients had at least one therapeutic aPTT
  • There were no patients who had all aPTT values within the therapeutic range during the first 48hours of UFH therapy
• Something to Think About: Thrombus burden can be substantial and heparin resistance may be present, so standard dosing may be inadequate in these patients
• My Opinion: LMWHs offer several advantages over unfractionated heparin including a longer half-life, increased bioavailability, and a more predictable dose response. In addition, LMWHs are dosed by weight, administered subcutaneously, and usually do not require dose adjustments or laboratory monitoring. Whereas unfractionated heparin is largely hepatically cleared, LMWHs are renally cleared
  • In 2017 [2], there was a Cochrane review that compared LMWH to UFH for the initial treatment of VTE. This included 29 RCTs with over 10,000 patients. The authors concluded that with moderate quality of evidence fixed dose LMWH reduced the incidence of recurrent thrombotic complications and occurrence of major hemorrhage during initial treatment with no difference in overall mortality compared to UFH
  • The 2019 European Society of Cardiology [3] also states: “LMWH and fondaparinux are preferred over UFH for initial anticoagulation in PE, as they carry a lower risk of inducing major bleeding and heparin-induced thrombocytopenia. Neither LMWH nor fondaparinux need routine monitoring of anti-Xa levels. Use of UFH is nowadays largely restricted to patients with overt hemodynamic instability or imminent hemodynamic decompensation in whom primary reperfusion treatment will be necessary. UFH is also recommended for patients with serious renal impairment [creatinine clearance ≤30mL/min] or severe obesity. If LMWH is prescribed in patients with CrCl 15 – 30mL/min, an adapted dosing scheme should be used.”

Author Conclusion: “The majority of patients with acute PE spend most of their first 48 hours outside of the therapeutic range of AC when treated with guideline standard dosing of UFH. Over half of the patients fail to achieve any therapeutic PTT level within 24 hours of UFH initiation, and no patient had all therapeutic aPTTs. Future research should focus on identifying factors associated with achieving therapeutic AC with UFH.”

Clinical Take Home Point: In this single center study of PERT team consulted PE patients standard dosing of UFH left most patients with a subtherapeutic aPTT level in the first 48 hours of treatment. Either we need to question the dosing regimen we use for UFH or we should consider switching to LMWH in the initial treatment of PE patients.

References:

1. Prucnal CK et al. Analysis of Partial Thromboplastin Times in Patients With Pulmonary Embolism During the First 48 Hours of Anticoagulation With Unfractionated Heparin. Acad Emerg Med 2020. PMID: 31625654
2. Robertson L et al. Fixed Dose Subcutaneous Low Molecular Weight Heparins Versus Adjusted Dose Unfractionated Heparin for the Initial Treatment of Venous Thromboembolism. Cochrane Database Syst Rev 2017. PMID: 28182249

Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami)

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Background: Nitrates can help improve symptoms and ischemia in the setting of acute myocardial infarction. Current teaching holds that nitrates should be avoided in patients with potential right ventricular myocardial infarction (RVMI), due to the risk of decreasing preload and precipitating hypotension. This belief is based on a single 1989 study of 40 patients with RVMI and endorsed by both the AHA and ESC guidelines [2].

In that 1989 study, of the 40 patients with RV infarction 20 had a decrease in blood pressure of ≥30mmHg and associated symptoms after the administration of nitrates (SL, Oral, Transdermal, or IV) and 20 did not. The conclusion of this paper was that inferior AMI with RV involvement has a strong association with hypotensive response to nitrates. The major issue is the study is limited by the fact that we are given no information on dosage and multiple routes of administration making clinical application difficult. Better data is needed to guide management.

REBEL Cast 124: Nitrates in Right Sided MIs?Click here for Direct Download of the Podcast

Paper: Wilkinson-Stokes M et al. Adverse Events From Nitrate Administration During Right Ventricular Myocardial Infarction: A Systematic Review and Meta-Analysis. Emerg Med J 2023. PMID: 36180168

Clinical Question: Is giving nitrates to patients with right ventricular myocardial infarction (RVMI) associated with increased adverse events compared with nitrate administration to patients with myocardial infarctions in other regions of the heart?

What They Did:

• A systematic review and meta-analysis
• Exposure of interest: administration of nitrates, via any route and dose

Outcomes:

• Primary: All forms of adverse events reported in the included studies (Hypotension, Bradycardia, AMS, Syncope, Cardiac Arrest)

Inclusion:

• Patients diagnosed with AMI with a subset of the sample with RV myocardial infarction
• Experimental and analytical observational study designs
• Studies only published in English

Exclusion:

• Patients with coronary vasospasm

Results:

• 5 studies included in the analysis
• Only 2 observational studies using SL NTG 400mcg were used for the meta-analysis
  • Adverse Events (Hypotension, Bradycardia, AMS, Syncope, Cardiac Arrest)
    • RVMI: 18/105 (17.1%)
    • Other MIs: 83/945 (8.8%)
    • RR 1.31 (95% CI 0.81 to 2.12)
    • No patients had cardiac arrest or death

Strengths:

• Asks a clinically important question
• Searched 6 different databases for relevant papers
• All included studies underwent quality assessment using standard appraisal tools
• If data was missing corresponding authors were contacted for the missing information

Limitations:

• None of the included studies were RCTs
• All studies samples were of combined inferior and RVMI making it difficult to determine the safety of nitrates during isolated RVMI
• One of the included studies was only an abstract
• Studies defined hypotension in different ways which could alter frequency of adverse events

Discussion:

• Overall this review provides low certainty evidence that there is no statistically significant difference in the rate of adverse events when nitrates are administered to RVMI compared with other cardiac region MIs.
• Hypotension is the primary adverse event reported. Nitrates have a serum half-life of 1 to 4 minutes and therefore hypotension is likely to be transient in nature
• Transient hypotension is not really clinically meaningful, especially since it can be treated with cessation of nitrates and fluid challenges

Author Conclusion: “This review suggests that the AHA and ESC contraindications are not supported by evidence. Key limitations include all studies having concomitant inferior and RVMI, not evaluating beneficial effects and very low certainty of evidence. As adverse events are transient and easily managed, nitrates are a reasonable treatment modality to consider during RVMI on current evidence.”

Clinical Take Home Point: From a clinical perspective, the potential benefit of analgesia and reduced sympathetic stimulation in the setting of RVMI seems to outweigh the potential of transient hypotension with the use of nitrates. Although better studies are needed, this systematic review and meta-analysis argues against a contraindication against nitrates in the setting of RVMI and maybe one of precaution.

References:

1. Wilkinson-Stokes M et al. Adverse Events From Nitrate Administration During Right Ventricular Myocardial Infarction: A Systematic Review and Meta-Analysis. Emerg Med J 2023. PMID: 36180168
2. Ferguson JJ et al. Significance of Nitroglycerin-Induced Hypotension with Inferior Wall Acute Myocardial Infarction. Am J Cardiol 1989. PMID: 2502902
3. Neumar RW et al. Part 1. Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015. PMID: 26472989
4. Ibanez B et al. 2017 ESC Guidelines for the Management of Acute Myocardial Infarction in Patients Presenting with ST-Segment Elevation. Eur Heart J 2018. PMID: 28886621

For More Thoughts on This Topic Checkout:

• REBEL EM: The Death of MONA in ACS – Part III – Nitroglycerin

Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami)

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REBEL Core Cast 119.0 – Sleep HygieneClick here for Direct Download of the Podcast

Employ sleep strategies:

• Anchor sleep: a period of sleep that overlaps each day regardless of your night shift schedule to provide a guidepost for your body clock. Ideally would overlap with when you would normally be asleep if you were not on night shift.
• Split sleep: sleep 3-4 hours immediately after shift then another 3-4 hours immediately before shift

Melatonin timing/dosing:

• Most sleep specialists recommend 1-3 mg 30 minutes before desired onset of sleep
• Align timing to bolster your circadian rhythm, not fight it

Caffeine:

• Limit intake 4-8 hours before bed and no more than 400 mg a day

Diet:

• Choose healthy foods and snacks and consume them in patterns that align with your normal day-night cycle (i.e. eat dinner before your night shift and eat breakfast afterwards)
• Residency/hospital leadership should consider having healthy low-cost/free food options available for residency and staff, particularly on night shifts

Don’t drive sleepy:

• Practice recognizing signs of sleep deprivation (yawning, drifting lanes, falling asleep at signout or at red lights) and do not drive home if present
• Residency/hospital leadership should provide a comfortable place for residents/faculty to sleep and/or provide rideshare options to safely get home when signs of sleep deprivation are recognized

References

Sleep strategies:

1. Minors DS, Waterhouse JM. Does ‘anchor sleep’ entrain circadian rhythms? Evidence from constant routine studies. J Physiol. 1983 Dec;345:451-67. doi: 10.1113/jphysiol.1983.sp014988. PMID: 6663508; PMCID: PMC1193807.
2. Crowley SJ, Lee C, Tseng CY, Fogg LF, Eastman CI. Complete or partial circadian re-entrainment improves performance, alertness, and mood during night-shift work. Sleep. 2004 Sep 15;27(6):1077-87. doi: 10.1093/sleep/27.6.1077. PMID: 15532201.

Melatonin

• Farahmand S, et al. Comparison of exogenous melatonin versus placebo on sleep efficiency in emergency medicine residents working night shifts: A randomized trial. World J Emerg Med. 2018;9(4):282-287. doi: 10.5847/wjem.j.1920-8642.2018.04.008. PMID: 30181797; PMCID: PMC6117540.
• Morgenthaler TI et al; Standards of Practice Committee of the American Academy of Sleep Medicine. Practice parameters for the clinical evaluation and treatment of circadian rhythm sleep disorders. An American Academy of Sleep Medicine report. Sleep. 2007 Nov;30(11):1445-59. doi: 10.1093/sleep/30.11.1445. Erratum in: Sleep. 2008 Jul 1;31(7):table of contents. PMID: 18041479; PMCID: PMC2082098.

Caffeine

1. Walsh JK, Muehlbach MJ, Schweitzer PK. Hypnotics and caffeine as countermeasures for shift work related sleepiness and sleep disturbance. J Sleep Res. 2009;4;80-83.
2. Nehlig A. Interindividual Differences in Caffeine Metabolism and Factors Driving Caffeine Consumption. Pharmacol Rev. 2018;70(2):384-411. doi:10.1124/pr.117.014407
3. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2020-2025. 9th Edition. December 2020. Available at DietaryGuidelines.gov.
4. Stephanie Centofanti, Siobhan Banks, Scott Coussens, Darren Gray, Emily Munro, Johnathon Nielsen & Jillian Dorrian (2020) A pilot study investigating the impact of a caffeine-nap on alertness during a simulated night shift, Chronobiology International, 37:9-10, 1469-1473, DOI: 10.1080/07420528.2020.1804922.

Diet

1. Lowden A, Holmbäck U, Åkerstedt T, Forslund J, Lennernäs M, Forslund A [2004]. Performance and sleepiness during a 24 h wake in constant conditions are affected by diet. Biol Psychol 65(3):251–263.
2. Anderson C, Horne JA [2006]. A high sugar content, low caffeine drink does not alleviate sleepiness but may worsen it. Hum Psychopharmacol 21(5):299–303.

Driving Sleepy

1. Barger LK, Cade BE, Ayas NT, et al. Extended work shifts and the risk of motor vehicle crashes among interns. N Engl J Med. 2005;352(2):125-34.
2. Green W, Gao X, Li K, et al. The Association of Sleep Hygiene and Drowsiness with Adverse Driving Events in Emergency Medicine Residents. West J Emerg Med. 2020;21(6):219-224. Published 2020 Oct 27. doi:10.5811/westjem.2020.8.47357
3. Steele MT, Ma OJ, Watson WA, Thomas HA Jr, Muelleman RL. The occupational risk of motor vehicle collisions for emergency medicine residents. Acad Emerg Med. 1999 Oct;6(10):1050-3. doi: 10.1111/j.1553-2712.1999.tb01191.x. PMID: 10530665.

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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REBEL Core Cast 118.0 – IM vs PO NSAIDsClick here for Direct Download of the Podcast

Bottom Line Up Top: There is no difference in analgesic efficacy between oral and intramuscular NSAIDs.

Clinical Scenario: A 34-year-old woman presents to the ED with back pain. After your history and physical, you conclude that the patient’s pain is muscular in origin and likely secondary to heavy lifting while moving apartments. You contemplate analgesic options and decide that a NSAID makes sense. Should you give her PO ibuprofen or IM ketorolac?

What Your Gut Says: Give the ketorolac IM. IM ketorolac will provide better pain relief and the patient will be happier with her care since she got an ‘injection’ and, after all, she did come all the way to the hospital.

What The Evidence Says: Unlike with many areas of medicine, there is ample evidence to answer this question and most of that evidence has been around for a couple of decades. Reviewing every study would be tedious and, fortunately, we’ve got a great review article on the topic. One important thing to understand is that the different NSAIDs have widely accepted equianalgesic doses; at the right dose, all NSAIDs (whether it be naproxen, ibuprofen, ketorolac or diclofenac) give equivalent pain relief (Irizarry 2021). This allows us to look at studies with the different NSAIDs and compare them to each other.

A 2007 review of the literature concluded that there was no difference in analgesia between IM ketorolac and PO ibuprofen (Arora 2007). The study included a number of high-quality research studies:

| Study | Format | Comparison | Findings | Notes | | Wright 1994 | Retrospective analysis of prospectively collected data. | PO Ibuprofen 800 mg vs IM ketorolac 60 mg | No difference in analgesic effect. | Ibuprofen superior secondary to cost, ease of administration + lack of pain w/ administration. | | Turturo 1995 | Double-blind RCT | PO Ibuprofen 800 mg vs IM ketorolac 60 mg | No difference in analgesic effect. | Similar onset of action in mild-moderate pain. | | Neighbor 1998 | Double-blind RCT | PO Ibuprofen 800 mg vs IM ketorolac 60 mg | No difference in analgesic effect. | | Mixter 1998 | Double-blind RCT | PO Ibuprofen 800 mg vs IM ketorolac 60 mg | No difference in analgesic effect. | Surgical Patients | | Quereshi 2019 | Double-blind RCT | IM diclofenac 75 mg vs PO diclofenac 100 mg | Small difference favoring IM in terms of speed to pain relief | Authors conclude PO superior due to time to prepare injection |

The data looks fairly clear in terms of analgesic efficacy but, don’t some patients simply prefer to receive a shot? While this dogmatic claim is often made, the data doesn’t appear to support it.

Schwartz and colleagues performed an ingenious trial (Schwartz 2000)

• Enrolled 64 ED patients with acute pain.
• Treatment arms:
  • Oral group: Orange drink (800 mg ibuprofen) + placebo “ibuprofen” pill
  • Injection group: Orange drink (800 mg ibuprofen) + placebo “ketorolac” injection
  • Essentially, all patients got the same analgesic medication (the orange drink) thinking it was just some juice and an inert study placebo (pill or injection).
• No significant difference in analgesia between the two groups.

Bottom Line: Just give the NSAID by mouth. IM NSAIDs may provide slightly faster time to analgesia but, IM dosing comes with the cost of injection, pain , a longer time to prepare the dose and more intensive nursing resources to administer the medication. As long as the patient’s gut works, oral NSAIDs provide similar analgesic effects to IM dosing and should be the preferred route of administration.

Bonus Pearls:

• IM injection of ketorolac causes significant pain. If the patient can’t take PO, be kind and pop in an IV.
• The ceiling pain relief dose for ketorolac is 15 mg IV (Motov 2017).

Read More

REBEL EM: The Ketorolac Analgesic Ceiling

References

Irizarry E et al. A randomized controlled trial of ibuprofen versus ketorolac versus diclofenac for acute, nonradicular low back pain. Acad Emerg Med 2021; 28(11): 1228-35. PMID: 34133820

Arora S et al. Myth: Parenteral ketorolac provides more effective analgesia than oral ibuprofen. Can J Emerg Med 2007; 9(1): 30-2. PMID: 17391598

Wright JM et al.. NSAID use and efficacy in the emergency department: single doses of oral ibuprofen versus intramuscular ketorolac. Ann Pharmacother 1994;28:309-12. PMID: 8193414

Turturro MA et a. Intramuscular ketorolac versus oral ibuprofen in acute musculoskeletal pain. Ann Emerg Med 1995;26:117-20. PMID: 7618770

Neighbor ML et al. Intramuscular ketorolac vs oral ibuprofen in emergency department patietns with acute pain. Acad Emerg Med; 1998; 5(2): 118-122 .PMID: 9492131

Mixter CG et al. Preemptive pain control in patients having laparoscopic hernia repair: a comparison of ketorolac and ibuprofen. Arch Surg 1998;133:432-7. PMID: 9565125

Qureshi I et al. Intramuscular versus oral diclofenac for acute pain in adults with acute musculoskeletal injuries presenting to the ED setting: a prospective, double-blind, double dummy, randomised controlled trial. 2019; 36: 401-6. PMID: 31217178

Schwartz NA et al. Patient’s perceptions of route of nonsteroidal anti-inflammatory drug administration and its effect on analgesia. Acad Emerg Med 2000; 7: 857-61. PMID: 10958124

Motov S et al. Comparison of intravenous ketorolac at three single-dose regimens for treating acute pain in the emergency department: a randomized controlled trial. Ann Emerg Med 2017; 70(2): 177-84. PMID: 27993418

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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Take Home Points

• Infections are a leading cause of maternal mortality worldwide.
• Prompt recognition is critical in management.
• Most infectious processes will require admission and close observation for improvement or decompensation.

REBEL Core Cast 117.0 – Infections of PregnancyClick here for Direct Download of the Podcast

Urinary Tract Infection/Pyelonephritis

Epidemiology:

• Occurs in as many as 15% of pregnant women and between 20-40% of pregnant women with asymptomatic bacteriuria will progress to pyelonephritis (Gorgas 2008)

Management:

• Uncomplicated UTI
  • Suggested antibiotics include:
    • Nitrofurantoin 100mg PO BID x7 days OR
    • Cephalexin 500mg PO BID x7 days
• Pyelonephritis
  • Hospital admission
  • Suggested antibiotics include:
    • Ceftriaxone 1g IV Q24H OR
    • Aztreonam 2g IV Q8H for beta-lactam allergy

Complications:

• Maternal sepsis
• Maternal renal injury
• Congenital abnormalities of the fetus
• Premature rupture of membranes
• Low birth weight

Chorioamnionitis

Definition: Also known as intraamniotic infection. Chorioamnionitis is a bacterial infection of fetal amnion and chorion membranes.

Epidemiology:

• Occurs in 1 to 10% of all pregnancies (Gorgas 2008)
• Incidence increases significantly with preterm labor

Diagnosis:

• Chorioamnionitis is defined as maternal fever >38°C and at least two of the following (Apantaku and Mulik 2007):
  • Maternal tachycardia >100 beats/min for five minutes
  • Fetal tachycardia >160 beats/min for five minutes
  • Purulent or foul-smelling amniotic fluid or vaginal discharge
  • Uterine tenderness
  • Maternal leukocytosis

Evaluation (Abbrescia 2003):

• CBC
• Blood cultures
• Vaginal fluid for phosphatidylglycerol
  • Tests for fetal lung maturity
• Cervical AND vaginal cultures
• Physical Exam
  • Avoid digital cervical exam
  • Speculum exam should be done with sterile speculum
• Ultrasonography for fetal well being

Management:

• Given concern for neonatal sepsis, patients should be admitted for IV antibiotics, supportive cares, and possible early delivery
• Most commonly an ascending infection from normal vaginal flora, so antibiotics must be chosen to cover polymicrobial infections
• Ex. Ampicillin IV 2g Q6H AND Gentamicin IV 1.5mg/kg Q8H
  • In PCN allergic patient substitute vancomycin 1 g IV Q12H for ampicillin
• Can only be considered cured with delivery of infected products of conception

Complications:

• Placental abruption
• Premature birth
• Neonatal sepsis
• Neonatal death
• Cerebral palsy
• Maternal sepsis
• Need for cesarean delivery
• Postpartum hemorrhage

Postpartum Endometritis

Definition: Generalized uterine infection

Epidemiology:

• Sepsis results in 15% of maternal deaths worldwide (Houry 2014)
• More common in surgical than vaginal deliveries
• May co-exist with surgical site infection

Diagnosis:

• Classic triad includes: fever, lower abdominal pain and uterine tenderness, and foul smelling lochia

Management:

• Hospital admission
• Cover for polymicrobial infection, including anaerobes
  • Ex. Clindamycin 900 mg IV Q8H AND Gentamicin 5-7 mg/kg IV Q24H

Septic Abortion

Epidemiology:

• The World Health Organization estimates that one in eight pregnancy related deaths worldwide can be directly attributed to unsafe abortion procedures (Gorgas 2008)

Diagnosis:

• Clinical presentation includes fever, abdominal pain and uterine tenderness in setting of recent abortion
• Presentation can vary from mild infection to septic shock

Evaluation:

• Lactate
• Cultures of cervix, blood and urine
• Coagulation panel to screen for DIC
• Abdominal X-ray to evaluate for free air or retained surgical foreign bodies
• Pelvic ultrasound to evaluate for retained products of conception or surgical foreign bodies

Management:

• Hospital admission may be indicated as infection can progress to septic shock, organ failure, DIC and cardiovascular collapse
• Broad-spectrum antibiotics are indicated. Triple antibiotic coverage is recommended. Suggested regimens include:
  • Ampicillin AND
  • Gentamicin AND
  • Clindamycin OR Metronidazole
• Update tetanus vaccination
• Usually requires dilation and curettage to remove any retained products of conception or foreign bodies.

References:

1. Abbrescia, K. and B. Sheridan (2003). “Complications of second and third trimester pregnancies.” Emerg Med Clin North Am 21(3): 695-710, vii. PMID: 12962354
2. Apantaku, O. and V. Mulik (2007). “Maternal intra-partum fever.” J Obstet Gynaecol 27(1): 12-15. PMID: 17365450
3. Desai, S. and S. Henderson. Labor and Delivery and Their Complications. In: Marx, J et al, ed. Rosen’s Emergency Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014:2331-2350.
4. Gorgas, D. L. (2008). “Infections related to pregnancy.” Emerg Med Clin North Am 26(2): 345-366, viii. PMID: 18406978
5. Houry, D and B. Salhi. Acute Complications of Pregnancy. In: Marx, J et al, ed. Rosen’s Emergency Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014: 2282-2299.

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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Background: Massive pulmonary embolism defined as sustained hypotension (SBP <90mmHg) has a high mortality which is why early recognition and thrombolytic therapy is typically recommended (AHA Class IIA; ESC Class IB) [1]. However, full-dose thrombolytic therapy (Alteplase 100mg (IV) is associated with an increase in bleeding [2]. Because the lungs receive 100% of cardiac output, it has been hypothesized that a lower dose of thrombolytic therapy may still be effective with a better safety profile [3][4].

REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE?Click here for Direct Download of the Podcast

Paper: Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358

Clinical Question: What is the efficacy and safety of low-dose (25mg) prolonged administration (over 6hrs) of alteplase in patients with massive PE?

What They Did: * Single-center, pilot prospective observational cohort trial in Turkey * Thrombolysis + 25mg of alteplase without a bolus was administered over 6 hours by peripheral IV infusion + If hemodynamic instability persisted despite first dose of thrombolysis, a second 6hr infusion of 25mg alteplase without bolus was administered (No patients in the study required this) + Did not use concomitant heparin anticoagulation with thrombolysis + Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed + Patients were all converted to warfarin for discharge * TTE + All patients underwent TTE before thrombolysis, within an hour after thrombolysis, before discharge (5 to 7d) and a month after thrombolysis + PASP estimated from tricuspid valve regurgitant jet velocity + Maximum dimension of RA/LA measured in 4-chamber view + Diameter and collapsibility of IVC noted + Pulmonary HTN defined as PASP >40mmHg + RV enlargement defined as RV/LV ratio >0.9 + Tricuspid Annular Plane Systolic Excursion (TAPSE) also recorded + Tissue Doppler Derived Tricuspid Annular Systolic Velocity recorded + Tei-Myocardial Performance Index (MPI/Tei) recorded * CT + All patients underwent 64 slice CTPA for definitive diagnosis of PE at admission + Additional CTPA 24 hours after completion of thrombolysis if eGFR >60mL/min/1.73m2 * Criteria for Thrombolytic Success Included: + Doppler documentation of resolution of increased PASP (<40mmHg) + Decreased RV diameter (at least 25% decrease of RV/LV diameter) + Restoration of RV function (TAPSE>16mm) + Systolic Wave Prime (S’) >10.0cm/s + Tissue Doppler Derived RV MPI > 0.55 + Clinical improvement of symptoms and restoration of stable hemodynamic status immediately after thrombolysis + Complete success = Clinical improvement of symptoms and restoration of a stable hemodynamic status along with at least 3 other criteria without resultant death and nonfatal major complications

Outcomes: Primary: + In-hospital mortality + Major complications - Ischemic stroke, ICH, embolism (coronary or peripheral), bleeding requiring transfusion - Pulmonary HTN while in hospital - RV dysfunction while in hospital + Secondary:* - 6 month mortality - Development of pulmonary hypertension at 6 months - RV dysfunction at 6 months

Inclusion:* Adult patients (≥18 years of age) * Confirmed massive PE + Massive PE Definition - Acute PE with sustained hypotension (SBP <90mmHg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or LV dysfunction) - Pulselessness - Persistent profound bradycardia (HR<40BPM with signs or symptoms of shock)

Exclusion:* Prior ICH * Known structural intracranial cerebrovascular disease (i.e. AV malformation) * Known malignant intracranial neoplasm * Ischemic stroke within 3 months * Suspected aortic dissection * Active bleeding or bleeding diathesis * Recent surgery encroaching on the spinal canal or brain * Recent significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury

Results:* 37 consecutive patients with massive PE were enrolled

• Blood pressure recovered within a few hours after initiation of thrombolysis in all cases
• Mortality
  • Primary Efficacy Outcome: 1 in-hospital death (3.1% in the paper but 2.7% in table 2) on day 6 of hospitalization due to malignant ventricular arrhythmia (Pt had ischemic dilated cardiomyopathy with LVEF of 20% and acute on chronic renal failure)
  • 2 additional deaths within 6 months (Both pts had malignancy)
  • Not implicitly stated whether these deaths are attributed to PE, however it doesn’t sound like they are based on the patient descriptions
• TTE Results from Admission to Post Thrombolysis:
  • Primary Efficacy Outcome: Mean PASP ≈57mmHg to 34mmHg (p<0.001)
    • Mean PASP continued to decrease prior to discharge ≈34mmHg to ≈30mmHg (p<0.001)
    • Mean PASP preserved at 6 month follow up ≈29mmHg
    • No patients with pulmonary hypertension at 6 months
  • Primary Efficacy Outcome: Mean TAPSE ≈1.43cm to 2.07cm (p<0.001)
  • RV/LV Diameter ≈1.37 to ≈0.99 (p<0.001)
  • Mean MPI/Tei Index≈ 0.47 to ≈0.55 (p<0.001)
  • Systolic Wave Prime (S’) ≈10 to ≈15
• Follow Up CTPA 24hrs After Thrombolysis
  • Out of 37 patients, 18 (56.3%) underwent repeat CTPA 24hrs after thrombolysis
    • Out of these 18 pts total lysis of thrombus was observed in 16pts (88.9%) and the remaining 2pts had >75% lysis of thrombus
  • Complications Post Thrombolysis:
    • Primary Safety Outcome: No major bleeding or stroke observed
    • 3 patients with minor bleeding
      • 2pts with epistaxis (2 days after thrombolysis)
      • 1pt with gingival bleeding (3 days after thrombolysis)
    • All bleeding events occurred during heparin infusion and stopped with gentle compression without recurrence
    • 6pts (17.6%) had major bleeding and 2pts (5.68%) had minor bleeding due to warfarin

Strengths:* Consecutive patients enrolled which minimizes selection bias * All patients followed for 6 months (No loss to follow up)

Limitations:* Single center, nonrandomized observational trial * No comparison group receiving standard therapy (i.e. compared to half-dose 50mg or full dose 100mg of alteplase) * Small sample size with few complications makes this an underpowered study to make any firm conclusions about bleeding risks * Lots of missing methodology + Unclear what time period patients were recruited + How strict were authors in consecutive recruitment (? selection bias) + Unclear therapies prior to lytics (i.e. Pressors, heparin, etc) + Who performed echos and unclear degree of consistency (Echo has some subjectivity to it)

Discussion: PE is a Spectrum of Disease + Massive PE is also a spectrum of disease + This study doesn’t appear to include critically ill massive PE patients who are peri-arrest + Dripping alteplase over 6 hours is most likely not going to be the appropriate therapy in the more severe massive PE patients * Primary Efficacy Outcome + Multiple primary efficacy outcomes were listed in this study, which can be problematic when you get multiple outcomes of varying statistical significance. In this trial all the primary efficacy outcomes were statistically significant, and the authors clearly defined what they meant by complete success in this trial * Complications While in Hospital + No cases of major bleeding or ICH in this study + The 3 patients who had minor bleeding at 48 to 72hrs were most likely due to the heparin infusion and not associated with thrombolysis + The cohort is simply too small with not enough complications for the study to be powered correctly for this outcome * IV Access + These authors gave alteplase through a peripheral IV which we do in stroke patients, but that is typically done over 1hr not over 6hrs + If I was going to do this (25mg alteplase over 6hrs) I would want a central venous catheter to avoid the potential of infiltration or if the patient decompensates further and needs central venous access after the fact there is a higher risk of hematoma/bleeding + Also, I would already have an arterial line in place before starting thrombolysis for continuous hemodynamic monitoring * Heparin Dosing + Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed + Prior studies have found marked increase in bleeding when lytics and heparin are given together + After thrombolysis I typically don’t bolus heparin and just start the infusion + Also I don’t start the heparin infusion immediately after thrombolysis, I wait for the PTT to be <2x the control before starting * A dose of 0.5 to 4.0mg/hr typically given in EKOS therapy (See Below). This trial gave 25mg over 6hrs (≈4mg/hr) + ULTIMA Trial [5]: - 59pts with massive/submassive PE - Used alteplase at a dose of 1mg/hr x5hrs, then 0.5mg/hr x10hrs - Max Dose ≈20mg - No major bleeding + SEATTLE II Trial [6]: - 150pts with massive/submassive PE - Used alteplase at a dose of 1mg/hr x24hrs - Max Dose ≈25mg - 1 severe/life-threatening hemorrhage (Groin hematoma requiring vasopressor support) - No ICH + OPTALYSE-PE Trial [7]:* - 101pts with submassive PE - Used alteplase at a dose of 8mg/2hrs (4mg/hr), 8mg/4hrs (2mg/hr), 12mg/6hrs (2mg/hr), and 24mg/6hrs (4mg/hr) - Max Dose 24mg - No major bleeding with 8mg/2hrs, 8mg/4hrs, and 12mg/6hrs - 2 major bleeding episodes occurred in the 24mg/6hr group + The max dose any patients got was ≈25mg (Max Dose Range ≈20mg to ≈25mg). Major bleeding seemed to occur in the drips that ran for over 15hrs (3 pts out of 310 [≈1%]); But no cases of major bleeding for drips ≤15hrs + To take this one step further this trial raises the question of whether EKOS even necessary or is it an overly expensive intervention that potentially increases complications without improving outcomes? * Although this was not a randomized clinical trial and there was no comparator arm we do have two trials on submassive PE with half-dose alteplase (50mg) given over 2hours [8] and half-dose alteplase (50mg) given in Massive PE [3] + MOPETT Trial [8] - 121pts with submassive PE (Called “moderate PE” in the study) - Randomized to half dose thrombolysis vs anticoagulation alone * For patients weighing ≥50kg a total dose of 50mg given (10mg bolus by IV push followed by 40mg infusion over 2hrs) * For patients weighing <50kg a total dose of 0.5mg/kg given (10mg bolus by IV push followed by the remainder over 2hrs) - Primary endpoints consisted of pulmonary HTN and composite of pulmonary HTN and recurrent PE at 28mos * Pulmonary HTN at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone * Composite Pulmonary HTN and Recurrent PE at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone - There were 0 cases of bleeding in either arm + PEAPETT Trial [3] - 23 patients with PEA cardiac arrest due to confirmed massive PE - All pts received 50mg of alteplase as an IV push while CPR was ongoing - ROSC occurred in 2 to 15 min after alteplase administration in all but one patient - There was no minor or major bleeding despite chest compressions + What this current trial [9] is really adding to the literature is an even lower dose of thrombolysis (25mg) efficacious? - We already know from the MOPETT trial [8] and PEAPETT trial [3] that half-dose alteplase (50mg) had zero cases of bleeding so this current trial just tells us what we already know. 25mg of alteplase has less risk of bleeding than 50mg of alteplase - Additionally, if 25mg can treat massive PEs [9], this could also be extrapolated to less severe high-risk submassive PEs (Although I would still love to see a head-to-head trial of 25mg vs 50mg)

Author Conclusion: “Results of this pilot study suggest that low-dose prolonged infusion of tPA is an effective and safe therapy in patients with massive PE. This protocol was also effective in decreasing PASP and restoration of RV function.”

Clinical Take Home Point: Low dose (25mg) alteplase given as a prolonged infusion (over 6hrs) is a promising effective and safe therapy in patients with massive PE and provides an alternative to full dose (100mg) and half-dose (50mg) alteplase. Larger RCTs comparing doses of alteplase are warranted to confirm these findings.

References:1. Jaff MR et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement from the American Heart Association. Circ 2011. PMID: 21422387 2. Wan S et al. Thrombolysis Compared with Heparin for the Initial Treatment of Pulmonary Embolism: A Meta-Analysis of the Randomized Controlled Trials. Circ 2004. PMID: 15262836 3. Sharifi M et al. Pulseless Electrical Activity in Pulmonary Embolism Treated with Thrombolysis (from the “PEAPETT” Study). AJEM 2016. PMID: 27422214 4. Wang C et al. Efficacy and Safety of Low Dose Recombinant Tissue-Type Plasminogen Activator for the Treatment of Acute Pulmonary Thromboemolism: A Randomized, Multicenter Controlled Trial. CHEST 2010. PMID: 19741062 5. Kucher N et al. Randomized, Controlled Trial of Ultrasound-Assisted Catheter-Directed Thrombolysis for Acute Intermediate-Risk Pulmonary Embolism. Circ 2014. PMID: 24226805 6. Piazza G et al. A prospective, Single-Arm Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism: The SEATTLE II Study. JACCC Cardiovasc Interv 2015. PMID: 26315743 7. Tapson VF et al. A Randomized Trial of the Optimum Duration of Acoustic Pulse Thrombolysis Procedure in Acute Intermediate-Reisk Pulmonary Embolism: The OPTALYSE PE Trial. JACC Cardiovasc Interv 2018. PMID: 30025734 8. Sharifi M et al. Moderate Pulmonary Embolism Treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol 2013. PMID: 23102885 9. Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358

For More Thoughts on This Topic Checkout: EMCrit:* EMCrit 354 – Reduced-Dose Systemic Peripheral Fibrinolysis in Massive Pulmonary Embolism

Post Peer Reviewed By: Anand Swaminathan, MD (X: @EMSwami)

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Take Home Points

• Achilles tendon rupture is a clinical diagnosis. The Thompson Test should be applied in all suspected cases.
• Remember to brace or splint a rupture, even if suspected, in the resting equinus position for optimal healing and prevention of further injury.
• Schedule follow up with orthopedics within 1 week for discussion of operative management vs early rehab protocols.

REBEL Core Cast 116.0 – Achilles Tendon RuptureClick here for Direct Download of the Podcast

Achilles Tendon Rupture Exam (www.lfaclinic.co.uk)Physical Exam

• May have palpable gap or deformity in region of tendon.
• Weakness with plantar flexion.
• Increased resting ankle dorsiflexion on affected side in prone position with knees bent .
• Usually in absence of bony tenderness unless accompanied by other injury
• Thompson Test(video)
  • Place the patient in the prone position, with feet hanging over the end of a stretcher or table. If patient is not able to lay down/there are no stretchers, the patient can kneel on a stool or chair
  • Squeeze the calf of the normal limb. You will notice the squeeze will cause the ankle to plantarflex appropriately
  • Squeeze the calf of the limb with the suspected Achilles tendon rupture. You will notice the squeeze will cause no motion if there is a full rupture/tear, and diminished motion if there is a partial tear
  • Performance Characteristics (Garras 2012)

| Sensitivity | Specificity | (+) LR | (-) LR | | 96-100% | 93-100% | 13.7 | 0.04 |

Imaging

• X-Rays
  • Used to rule out other or concurrent pathology
  • May show soft tissue swelling and destruction of pre-Achilles fat pad (Kager’s Fat Pad)
  • Findings are non-specific as tear of tendon unable to be visualized
• Ultrasound
  • Ultrasound is helpful if obvious findings present and to distinguish between partial vs complete tears, however only around 50% sensitive for detecting only partial tears (Kayser 2005)
• MRI
  • Gold-standard imaging modality
  • Rarely, if ever, necessary in the ED
  • Used for equivocal physical exam/alternate imaging findings or for assessing the severity of the tear for possible operative management
  • Findings
    • A full-thickness tear often shows a tendinous gap filled with edema or blood
    • Complete rupture shows retraction of tendon ends

ED Management

• • Provide analgesia
  • Tendon stabilization in an optimal healing position
    • Functional bracing/splinting in resting equinus/talipus equinus
    • AO splint/brace in 20 degrees of plantar flexion for 4-6 weeks (may use tall CAM boot with 20 degrees wedge inserts)
    • All patients should be non-weightbearing
      • Any weight-bearing can convert a partial tear to a complete tear
      • Maintain non-weightbearing status until see orthopedics (within 1 week)
      • After evaluation by orthopedics, early weight-bearing and early ROM exercises yield better outcomes (can be as early as 2 weeks)
• Referral to rehab warranted to improve plantar flexion and decrease risk of re-rupture
  • ED Ortho consultation: patients with open wounds in the area of trauma, or with concomitant fractures
  • Operative Management is usually reserved for acute ruptures (approximately <6 weeks) of full thickness with large tendon gaps, failed conservative treatment of partial thickness tears, or high performance athletes
    • These cases will be determined during follow up with orthopedics and may warrant outpatient MRI to assess severity of tear

Prognosis

• • For conservative management, there is no significant difference in plantar flexion strength (Willits, 2010)
  • Some increased risk of re-rupture compared to operative management, although review of evidence shows that this may not be significant if patients used structured, accelerated rehab protocol.
    • Protocol includes initially non-weightbearing cast with the foot in equinus position as described above, then transitioned to a pneumatic walker with elevated heels (elevation gradually reduced biweekly), and physical therapy to improve gait, strength, and mobility. (Wallace 2011)
  • If addressed early and appropriately, most patients have good self-reported long-term outcomes regardless of the treatment modality

Links

Orthobullets:Achilles Tendon Rupture

Resources:

• Sheth U et al. The epidemiology and trends in management of acute Achilles tendon ruptures in Ontario, Canada: a population-based study of 27,607 patients. Bone Joint J. 2017; 99-B(1): 78-86. PMID: 28053261
• Chiodo CP, Wilson MG. Current Concepts Review: Acute Ruptures of the Achilles Tendon. Foot Ankle Int 2006; 27(4): 305-13. PMID: 16624224
• Leppilahti J, Orava S. Total Achilles tendon rupture. A review. Sports Med. 1998; 25(2): 79-100. PMID: 9519398
• Kayser R et al. Partial rupture of the proximal Achilles tendon: a differential diagnostic problem in ultrasound imaging. Br J Sports Med. 2005; 39(11): 838-42. PMID: 16244194
• Margetic P et al. Comparison of ultrasonographic and intraoperative findings in Achilles tendon rupture. Coll Antropol. 2007; 31:279-284. PMID: 17598414
• Garras DN et al. MRI is Unnecessary for Diagnosing Acute Achilles Tendon Ruptures: Clinical Diagnostic Criteria. Clin Orthop Relat Res 2012; 470(8): 2268-2273. PMID: 22538958
• Willits K et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial using accelerated functional rehabilitation .J Bone Joint Surg Am. 2010; 92(17): 2767-75. PMID: 21037028
• Wallace RG et al. The non-operative functional management of patients with a rupture of the tendo Achillis leads to low rates of re-rupture. J Bone Joint Surg Br 2011; 93(10):1362-6. PMID: 21969435
• Erickson BJ. Is Operative Treatment of Achilles Tendon Ruptures Superior to Nonoperative Treatment? Orthop J Sports Med. 2015; 3(4): PMID: 26665055

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

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Take Home Points:

• Know clinical (cold extremities, oliguria, confusion, dizziness, narrow pulse pressure) and laboratory markers (metabolic acidosis, elevated creatinine, lactic acidosis) of hypoperfusion.
• An elevated lactate is a danger sign and requires explanation.
• Norepinephrine is a great first line vasopressor in Cardiogenic shock.
• Dobutamine is useful for inotropic support in Cardiogenic shock.
• Use POCUS in ED. In addition to echo and VTI for cardiac output, use IVC assessment for central venous pressure/volume status.

REBEL Core Cast 115.0 – Cardiogenic ShockClick here for Direct Download of the Podcast

Links

Staten Island EM: Only in Staten Podcast

Links: VTI Calculation on Echo: https://www.youtube.com/watch?v=ir5EusiBXhk

Post Created By: Anand Swaminathan MD, MPH

Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)

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Take Home Points: Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters. The symptoms of mild, acute exposure are non-specific and can be confused with a variety of ... Read more

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Take Home Points: All STEMIs should be loaded with dual antiplatelet therapy. Prasugrel (Effient) is avoided as there is an increase in bleeding complications if the patient requires a CABG. NSTEMI cases can be challenging to manage. Consult Cardiology early and use all available data. The appropriate medical treatment for ACS patients is as important ... Read more

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Take Home Points: Dose your RSI meds correctly. Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic. Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor! REBEL Core Cast 112.0 – Awareness During ... Read more

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Take Home Points: A CCTA is an anatomic test to determine if a patient has normal coronary arteries, non-obstructive disease, or obstructive disease. The warranty period for a CCTA is anywhere from 3-10 years depending on the characteristics of the plaque. A nuclear stress test is a functional study that allows for ischemia-driven management. The ... Read more

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Take Home Points: Patients with recent onset atrial fibrillation can safely be cardioverted if they are 1) on anticoagulation 2) Low risk based on CHADS-VASC with onset < 48 hours or 3) High risk based on CHADS-VASC with onset < 12 hours. In anaphylaxis, think, “If A, B or C, give E.” If the patient ... Read more

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Take Home Points: In the context of poisoning, a “wide QRS” is anything greater than 100 milliseconds. A newly “wide QRS”, especially with hemodynamic instability, should prompt consideration of sodium channel blockade and not ventricular tachycardia. Treatment is guided by administration of sodium-bicarbonate. Recall that the resultant alkalemia driven by sodium-bicarbonate will shift potassium intracellularly. ... Read more

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Take Home Points: Airway management is paramount; expect a challenging intubation and consider controlling the airway early if there is apparent airway compromise. Understanding the cause of angioedema (mast cell vs. bradykinin mediated) helps dictate directed management. Urticaria and pruritus = MAST CELL mediated, which is treated like a standard allergic reaction. REBEL Core Cast ... Read more

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Take Home Points Clinical presentation is very nonspecific; evaluate all patients presenting with back pain for infectious risk factors. Baseline labs should not guide diagnosis, but may assist in later management. MRI is key to diagnosis, obtain this imaging in all patients who raise clinical suspicion Patients with hemodynamic instability and neurologic compromise warrant empiric ... Read more

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Take Home Points REBEL Core Cast 106.0 – Nerve Block Basics Click here for Direct Download of the Podcast Resources REBEL EM: Local Anesthetic Systemic Toxicity Sono in Staten Blog: https://www.statenislandem.com/sono-in-staten Core Ultrasound: https://www.coreultrasound.com/ POCUS Atlas: https://www.thepocusatlas.com/ Highland Ultrasound: http://highlandultrasound.com/ Post Created By: Billy Caputo MD Post Peer Reviewed By: Anand Swaminathan MD, MPH (Twitter ... Read more

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Background: Getting a definitive airway in a critically ill trauma patient can be a stressful situation. The potential for soiled airways, cervical spine injuries, maxillofacial injuries and head injuries combined with agitation/delirium, altered mental status and hypoxemia can make securing a definitive airway both an anatomic and physiologic challenge. Traditional RSI entails preoxygenation followed by ... Read more

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Background: The ongoing debate between video laryngoscopy (VL) and direct laryngoscopy (DL) has ignited intense debate within the emergency medicine and critical care communities. A recent pragmatic, randomized, multicenter trial (The DEVICE Trial) compared the two techniques to determine if VL outperformed DL in first-pass success (FPS). In this blog post, we explore the study’s ... Read more

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Take Home Points Methylxanthines are a drug class that includes caffeine, theophylline, and theobromine. The three main mechanisms that account for the clinical presentation of methylxanthine toxicity are: catecholamine release, adenosine antagonism, and phosphodiesterase inhibition. Beta agonism will lead to hyperlactatemia, hypokalemia, hyperglycemia, and tachycardia. Adenosine antagonism may lead to seizures and/or supraventricular tachycardia that ... Read more

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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

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Take Home Points Provider assessment of how the patient looks is extremely important. If it looks and feels like a STEMI clinically, get serial ECGs and consult Cardiology immediately. POCUS has been a phenomenal tool in the management and early diagnosis of a lot of abnormal ECG and chest pain presentations. Isolated elevation in aVR ... Read more

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Back on June 1st, 2023, Swami wrote a blog post on REBEL EM titled, The CT FIRST Trial, Should We Pan-CT After ROSC?. This stemmed a lot of discussion in the background between Swami, myself, and Scott. We felt it was worthwhile to record this as a podcast to better flush out some nuanced points. ... Read more

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Background: Hemorrhage is the leading cause of mortality in trauma patients. Interventions such as early application of hemorrhage control, tranexamic acid, reduction of crystalloid fluid administration and balanced ratio blood product transfusion have improved many patients’ outcomes. However, mortality still remains high due to trauma-induced coagulopathy. Some clinicians have advocated for early administration of 4-factor ... Read more

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Take Home Points Caustics are substances that injure tissue upon physical contact. Caustic potential is not purely a function of pH. The decision to admit is dependent on the history and physical. Vomiting, drooling, and stridor are concerning. Stridor alone or 2/3 symptoms should warrant admission and gastroenterology consultation for potential endoscopy. The lack of ... Read more

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Background Information: Opioid overdose deaths have been increasing in the past twenty years. The national number of overdose deaths from any opioid has increased 62.5% from 2019 to 2021 (from 48,000 to 81,400 annual deaths), which includes prescription opioids (natural and semi-synthetic opioids and methadone), heroin, and synthetic opioids other than methadone including fentanyl (1). Opioid ... Read more

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Take Home Points

1. The Parkland formula can be used to be a guide for initial fluid resuscitation. This is based on second- and third-degree burns (not first-degree). Utilize response to treatment as a guide to continue fluid resuscitation.
2. Patients in fires in closed spaces for a prolonged time are at risk for airway edema and need for intubation. History of fire is very important and please monitor patient condition, patients’ voice, and repeat physical exam.
3. Prophylactic antibiotics can be avoided in most burn cases.
4. Checking extremity pulses for extremity burns are important. Loss of pulse should trigger an escharotomy. Continued loss of pulse should trigger a fasciotomy.
5. Have a low threshold for starting Hydroxocobalamin for possible cyanide toxicity and for testing for a carboxyhemoglobin level for possible carbon monoxide toxicity.

REBEL Core Cast 102.0 – Burn ManagementClick here for Direct Download of the Podcast

Check out the “Only in Staten” Podcast

Post Created By: Anand Swaminathan MD, MPH + Billy Caputo MD

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Background: IV fluids are part of the standard resuscitation bundle in septic shock, however it is unclear if they provide a significant benefit. These patients can have a vasodilated vascular bed and the initial use of fluids is hypothesized to serve two purposes: Augmenting the macrovascular system (stroke volume and cardiac output) and augmenting the microvascular perfusion (capillary blood flow). However, IV fluids are not a benign intervention as they can cause coagulopathy and fluid overload.

The CENSER Trial (Link is HERE) was a randomized, double-blind, placebo-controlled clinical trial evaluating the use of early low-dose norepinephrine vs standard care (placebo) in adults with septic shock. The goal of the trial was to see if early vasopressors improved shock control by 6 hours. Patients were started on low-dose norepinephrine at a median time from ED arrival of 93 minutes compared to 192minutes in the standard care arm. This resulted in better shock control by 6hrs (76.1% vs 48.4%). The secondary outcome of mortality was not statistically different however numerically favored the early use of norepinephrine.

Physiologically it makes sense to initially use lower volumes of fluids and earlier initiation of vasopressors. However, there is a lack of robust evidence to help guide what fluid and vasopressor strategy is best in patients with septic shock.

REBEL Cast Ep116: The CLOVERS Trial – Restrictive vs Liberal Fluids in Sepsis-Induced HypotensionClick here for Direct Download of the Podcast

Paper: The National Heart, Lung and Blood Institute Prevention and Early Treatment of Acute Lung Injury Clinical Trials Network. Early Restrictive or Liberal Fluid Management for Sepsis-Induced Hypotension. NEJM 2023. PMID: 36688507 [Access on Read by QxMD]

Clinical Question: In patients with sepsis-induced hypotension, after an initial 1 to 3L of IV crystalloids, does using a restrictive fluid strategy improve 90d all-cause mortality compared to a liberal fluid strategy?

What They Did: * Crystalloid Liberal or Vasopressor Early Resuscitation in Sepsis (CLOVERS) * Multicenter, unblinded, randomized, superiority clinical trial conducted at 60 US centers * Randomization occurred within 4 hours after patients met the criteria for sepsis-induced hypotension refractory to initial treatment with 1 to 3L of IV fluid * Patients randomized 1:1 to one of two arms for a 24 hour period: + Restrictive Fluid Strategy: Prioritizing vasopressors and lower IV fluid volumes; Rescue fluids were allowed + Liberal Fluid Strategy: Prioritizing higher volumes of IV fluids before vasopressor use; Recommended initial 2000cc of isotonic crystalloid followed by fluid boluses based on clinical triggers + In October 2019 a protocol amendment was made allowing for limited initial infusion of crystalloids to 1000cc if patients’ blood pressure and heart rate had been stabilized (SBP ≥110mmHg or MAP ≥70mmHg and HR <90BPM) and patient was volume replete (unlikely to benefit from additional IV fluids)

Outcomes: Primary: All -cause mortality before discharge home by 90d * Secondary: + Number of days free from ventilator at 28d + Days free from renal-replacement therapy at 28d + Days free from vasopressor use at 28d + Days of the ICU at 28d + Days out of the hospital at 28d * Safety:* + Initiation of mechanical ventilation + New onset atrial and ventricular arrhythmias + Complications related to peripheral and central venous catheter use

Inclusion:* Adult (≥18 years of age) patients * Suspected or confirmed infection * Sepsis-induced hypotension (SBP <100mmHg after administration of ≥1000mL of IV fluids)

Exclusion:* >4hrs since meeting criteria for hypotension refractor to IV fluids of at least 1000cc * >24hrs since presentation to the hospital * Previous receipt of >3000cc of IV fluids * Presence of fluid overload * Presence of severe volume depletion from nonsepsis causes

Results:* 1563 patients enrolled * Resuscitation therapies administered prior to randomization were similar between two groups: + Restrictive: Median 2050mL (Range: 1500 to 2457mL) + Liberal: Median 2050mL (Range: 1371 to 2442mL) * Median time from meeting trial eligibility criteria to randomization: 61min (No real difference between groups) * Majority of patients were randomized from the ED: 91.9% of enrolled patients * Resuscitation therapies administered during the 24hr protocol period differed between the two groups: + Restrictive fluid strategy group received less fluids than the liberal fluid strategy group (Median difference: -2134mL; 95% CI -2318 to -1949) + Restrictive fluid strategy group received earlier, more prevalent, and longer duration of vasopressors vs the liberal fluid strategy group * Median Volume of Fluid During 1st 6 Hours After Randomization: + Restrictive: 500mL (Range 130 to 1097mL) + Liberal: 2300mL (Range 2000 to 3000mL) + Difference: -1800mL + This difference remained for the 1st 24hrs after randomization as well (1267mL vs 3400mL) + The difference also remained for the 1st 24hrs after randomization when including fluids administered pre-enrollment: 3300mL vs 5400mL + Most common fluid type used was Lactated Ringer’s Solution * Vasopressor Use in the 1st 24hrs After Randomization: + Restrictive: 59% + Liberal: 37% + Also initiated earlier (mean difference -1.4hrs) and used for longer (mean difference 4.2hrs) * 90d All-Cause Mortality: + Restrictive: 14.0% + Liberal: 14.9% + Estimated Difference: -0.9%; 95% CI 04.4 to 2.6; p = 0.61 + Prespecified subgroup analyses did not show differences in treatment effects (Included SBP <90mmHg, Chronic Heart Failure, ESRD, Pneumonia as Cause of Sepsis) * Number of reported serious adverse events were similar between groups

Strengths:* Asked a clinically important question * Primary outcome was objective (i.e. mortality) * Monitored protocol adherence in the first 300 patients and in a 10% random sample of patients throughout the rest of the trial * Groups had similar baseline characteristics and treatment before randomization * Audited protocol adherence was high in both groups with overall adherence of 97% in the restrictive group and 96% in the liberal group. Adherence was sustained throughout the duration of the trial * Authors achieved separation between groups in terms of the amount of fluid given between both strategies

Limitations: Convenience sample of enrolled patients mostly during weekdays may have caused a selection bias (Only enrolled ≈1500 patients from 60 hospitals over a near 4 year period). * Also ≈3300 eligible patients screened of which many not enrolled. 900 patients could not get informed consent, ≈880 patients refused consent, ≈880 patients the MD refused to enroll, and ≈350 not excluded but not enrolled * Excluded patients with extremes of volume overload or volume depletion which makes drawing conclusions in these populations not possible * Although there was high adherence to the protocol, some patients in the restrictive fluid group received more fluid than was intended and vasopressors were started later than intended. Additionally, some patients in the liberal fluid group received less fluid than was intended and vasopressors were started earlier than was intended. Both of these protocol violations could have diluted the difference between groups * Unblinded trial: Clinical team was aware of which group patients were randomized to. This could have influenced care the patients received as well as reporting of adverse events (i.e. higher reporting of volume overload in the liberal fluid group or lesser reporting of volume overload in the restrictive fluid group) * Goals of care were driven by blood pressure and lactic acid targets. It is unclear if outcomes would have differed with different targets or allowing for lower blood pressure values * Trial protocol was only for 24 hours after randomization. It is unclear if a longer treatment period would have produced differing results * Study terminated early which did not allow authors to achieve the appropriate statistical power required to find a between group difference of 4.5% in the incidence of death before discharge home by day 90. Even if the authors had completed the trial with the remaining patients having good outcomes in the restrictive strategy group, this trial still may not have reached statistical significance. * The patients enrolled didn’t seem that sick (Baseline SBP 93.5mmHg and Lactic Acid of 2.9) with only* ≈60% of patients in the restrictive group requiring vasopressors at all. Additionally, mortality rate was ≈14% in this trial (Compared to ProCESS 19%, ARISE 18.5%, and ProMISe ≈29%).**

Discussion: Authors were looking for an absolute between-group difference of 4.5% in the incidence of death before discharge home by day 90 (Primary outcome) assuming death would occur in 15% of patients in the liberal fluid group and 10.5% in the restrictive fluid group. This would require a sample of 2320 patients to be enrolled to achieve a 90% power (Trial did not reach this number as the trial was terminated for futility after 2/3rds of patients enrolled) * 3 instances of vasopressor extravasation among 500 patients who received peripherally administered vasopressors between randomization and 72hrs; All 3 events resolved without intervention and did not have any residual clinical consequences * My biggest issue not only with this study, but even previous trials is lumping sepsis patients into one group as if they are all the same. Sepsis is a heterogenous process with different causes, and different responses by patients. Clinical judgement is still alive and well…one protocol will not work for a heterogenous disease process.*

Author Conclusion: “Among patients with sepsis-induced hypotension, the restrictive fluid strategy that was used in this trial did not result in significantly lower (or higher) mortality before discharge home by day 90 than the liberal fluid strategy.”

Clinical Take Home Point: In a group of patients with septic shock (sepsis-induced hypotension), receiving initial treatment with 1 to 3 liters of IV fluids, a restrictive fluid strategy (with early vasopressor use) did not result in a significantly lower (or higher) mortality before discharge home by day 90 compared to a liberal fluid strategy. Basically, in a heterogenous disease process like sepsis, use your clinical judgement to determine how much fluid any particular patient needs.

References:1. The National Heart, Lung and Blood Institute Prevention and Early Treatment of Acute Lung Injury Clinical Trials Network. Early Restrictive or Liberal Fluid Management for Sepsis-Induced Hypotension. NEJM 2023. PMID: 36688507 [Access on Read by QxMD]

For More Thoughts on This Topic Checkout: The Bottom Line: CLOVERS * First10EM: The CLOVERS Trial – Does Nothing Matter in Sepsis * FOAMcast: CLOVERS Trial – Restricted vs Liberal Fluids in Sepsis-Induced Hypotension * REBEL EM: The CENSER Trial – Early Norepinephrine in Septic Shock * EMCrit:* EMCrit 345 – I Guess We Need to Talk About CLOVERS and Fluids in Sepsis (Hopefully for the Last Time Ever)

Post Peer Reviewed By: Anand Swaminathan, MD (Twitter: @EMSwami)

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Take Home Points

1. Many patients with renal colic require a CT scan.
2. Diagnostic imaging should focus on eliminating concerning mimics; not on clinching the diagnosis of renal colic.
3. POCUS and radiology department US are important modalities in evaluation of renal colic.

REBEL Core Cast 101.0 – Imaging in Renal ColicClick here for Direct Download of the Podcast

References: Moore CL et al. Imaging in suspected renal colic: systematic review of the literature and multispeciality consensus. Ann Emerg Med 2019; 74: 391-9. PMID: 31412438 * Corependium: Renal Stone Disease * REBEL EM: Kidney Stone Tag * Post Created By: Anand Swaminathan MD, MPH * Post Peer Reviewed By:* Salim R. Rezaie, MD (Twitter: @srrezaie) The post REBEL Core Cast 101.0 – Imaging in Renal Colic appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points

1. Alcoholic Ketoacidosis (AKA) can present with significant acidemia (pH < 7.00). Despite the significant acidemia, patients with AKA can remain alert and lucid despite their severe metabolic derangement.
2. Relying on urine ketones for diagnosis can be misleading, as acetoacetate is the primary ketone detected in the urine but not the most common ketone generated in AKA. Given the redox ratio in patients with severe ethanol use disorder, urine ketones may be low or negative, as beta-hydroxybutyrate is the predominant ketone body.
3. Treatment consists of thiamine, dextrose, and volume repletion.
4. Remember to evaluate for concurrent medical illness: gastritis, pancreatitis, pyelonephritis, pneumonia, sepsis.

REBEL Core Cast 100.0 – Alcoholic KetoacidosisClick here for Direct Download of the Podcast

Definition and Physiology

• Alcoholic ketoacidosis is a starvation state that occurs in the patient with severe ethanol use disorder.
• The normal response to starvation is to utilize hepatic glycogen stores in order to generate glucose.
  • In patients with severe ethanol use disorder who are malnourished, fatty acids and proteins are broken down to generate ketone bodies which are utilized by both the brain and heart.
• Note that the metabolism of ethanol increases the NADH:NAD+ ratio. This in turn diverts pyruvate to lactate (accounting for the presence of lactate in this population) and inhibits gluconeogenesis. As a result, patients with AKA tend to presents with a low or low/normal glucose concentration.

Clinical Manifestations

• Typical presentation: nausea, vomiting, and abdominal discomfort in the context of poor nutritional intake in a patient with ethanol use disorder.
• Physical examination
  • Kussmaul breathing (in order to compensate for a severe metabolic acidosis). However, in contrast to other cases of respiratory compensation, there is a tendency for patients presenting with AKA to maintain their mental status and remain lucid.1
  • Tachycardia may be present due to significant volume loss.
  • Evaluate for concurrent Wernicke’s Encephalopathy: classic triad of encephalopathy, ophthalmoplegia (classically nystagmus and lateral rectus palsy), and ataxia.2
• Ethanol concentrations may be low or undetectable. Glucose concentrations may be low or normal. Other electrolyte abnormalities including hypokalemia and hypomagnesemia can be found.
• Severe metabolic acidemia can occur which is out of proportion compared to the patient’s clinical presentation. pH < 7.00 has been reported.3

Diagnosis

• High Pre-Test Probability Patient: poor PO intake in a patient with ethanol use disorder
• Metabolic Acidemia + Lactate
• +Beta-Hydroxybutyrate

Management

• Sufficient dextrose containing crystalloid replacement in order to restore volume loss. (D5/NS or D5/LR)
• Oral nutrition if patient is able to tolerate. If not, dextrose containing fluids will suffice.
• Thiamine 100mg IV4
• Fix electrolyte abnormalities (Hypokalemia, Hypomagnesemia)
• Administration of bicarbonate is generally unnecessary.

Take Home Points

1. Alcoholic Ketoacidosis (AKA) can present with significant acidemia (pH < 7.00). Despite the significant acidemia, patients with AKA can remain alert and lucid despite their severe metabolic derangement.
2. Relying on urine ketones for diagnosis can be misleading, as acetoacetate is the primary ketone detected in the urine but not the most common ketone generated in AKA. Given the redox ratio in patients with severe ethanol use disorder, urine ketones may be low or negative, as beta-hydroxybutyrate is the predominant ketone body.
3. Treatment consists of thiamine, dextrose, and volume repletion.
4. Remember to evaluate for concurrent medical illness: gastritis, pancreatitis, pyelonephritis, pneumonia, sepsis.

References

1. Wrenn KD, Slovis CM, Minion GE, Rutkowski R. The syndrome of alcoholic ketoacidosis. Am J Med. 1991 Aug;91(2):119-28. doi: 10.1016/0002-9343(91)90003-g. PMID: 1867237.
2. https://coreem.net/core/wernicke-encephalopathy/
3. Fulop M, Hoberman HD. Alcoholic detosis. Diabetes. 1975 Sep;24(9):785-90. doi: 10.2337/diab.24.9.785. PMID: 808436.
4. https://coreem.net/core/alcoholic-ketoacidosis/

Post Created By: Sanjay Mohan, MD

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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REBEL Core Cast 99.0 – Bundle Branch BlocksClick here for Direct Download of the Podcast

Cardiac Conduction System (LITFL)Definition: Interruption of the normal conduction system leading to aberrant conduction and an abnormal QRS morphology

Anatomy: At the AV node, conduction splits into the right and left bundle branches. The left bundle branch is composed of anterior and posterior branches.

Right Bundle Branch Block (RBBB)

Physiology

• Normally, the right bundle depolarizes the right ventricle (RV)
• In a RBBB, the right bundle does not activate. The right ventricle is instead depolarized by spread of impulse from the left bundle, through the left ventricle (LV) and then to the RV
• This pattern of electrical spread creates an aberrant QRS morphology
• Depolarization vector produces delayed R waves in leads V1-3 and delayed S waves in the lateral leads.

RBBB Criteria

• Rhythm is supraventricular in origin
• QRS duration > 110 msec (some criteria state > 120 msec)
• Terminal R wave in lead V1 giving an RSR’ morphology (i.e. “Rabbit Ears”)
• Wide terminal S wave in leads I, aVL, V5 and V6
• Axis is normal.

RBBB (LITFL)Note: A partial RBBB, defined as a RBBB morphology with a QRS < 100 msec, can be pathologic (i.e. in right heart strain) or a normal variant (seen in up to 10% of the general population)

Incomplete RBBB (LITFL)Left Bundle Branch Block (LBBB)

Physiology

• The left bundle is composed of two fascicles (the left anterior and the left posterior fascicle)
• Normally, the left bundle depolarizes the left ventricle
• In a LBBB, the left bundle does not activate. The left ventricle is, instead, depolarized by spread of impulse from the right bundle through the RV and then to the LV.
• This pattern of electrical spread creates an aberrant QRS morphology
• The left bundle has two fascicles (anterior and posterior) and either (or both) can have a conduction abnormality

LBBB Criteria

• Rhythm is supraventricular in origin
• QRS duration > 120 msec
• QS or rS morphology in lead V1 + V2
• Broad, dominant monomorphic R wave in lead I, aVL, V5 and V6

LBBB (LITFL)Fascicle Blocks

LAFB EKG (LITFL)Left Anterior Fascicular Block (LAFB aka left anterior hemi-block)

• Blocking the left anterior fascicle results in LV depolarization via the left posterior fascicle which inserts into the infero-septal wall of the LV
• Produces small R waves in II, III, aVF
• Produces tall R waves in left-sided leads and deep S waves in the inferior leads
• LAFB EKG Criteria
  • Left axis deviation (QRS up in I, down in II + aVF)
  • Slight prolongation of the QRS complex (but < 120 msec)
  • Small q waves and large R waves (qR complexes) in leads I and aVL
  • Small r waves and large S waves (rS complexes) in leads II, III + aVF
• Causes of LAD
  • LAFB
  • LBBB
  • LV Hypertrophy
  • Inferior MI
  • Ventricular ectopy
  • Paced rhythm
  • WPW

LAFB Annotated (REBEL EM)LPFB EKG (LITFL)Left Posterior Fascicular Block (LPFB aka left posterior hemi-block)

• Blocking the left posterior fascicle results in LV depolarization via the left anterior fascicle which inserts into the upper, lateral wall of the LV
• LPFB is much less common than LAFB and the LAFB typically occurs with a RBBB (bifascicular block)
• LPFB EKG Criteria
  • Right axis deviation (RAD) (QRS up in III + aVF, down in I)
  • Slight prolongation of the QRS complex (but < 120 msec)
  • qR complexes in leads II, III + aVF
  • rS complexes in leads I + aVL
  • No evidence of RV hypertrophy
  • No evidence of other cause of right axis deviation
• Causes of RAD
  • LPFB
  • Old lateral myocardial infarction
  • Acute pulmonary hypertension (e.g. pulmonary embolism)
  • Chronic pulmonary hypertension
  • Sodium channel blocking drugs
  • Hyperkalemia
  • Right ventricular hypertrophy
  • Misplaced leads

LPFB Annotated (REBEL EM)Post Created By: Anand Swaminathan MD, MPH

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Background information: Alcohol has potentiating effects on the inhibitory GABA neurotransmission system and inhibitory effects on the excitatory glutamate neurotransmission system. Chronic alcohol use causes changes to preserve homeostasis, and when the stimulus is removed, alcohol withdrawal results due to decreased inhibition via the GABA system and increased excitation via the glutamate system. Treatment options for alcohol withdrawal include benzodiazepines such as lorazepam, diazepam, or chlordiazepoxide, gabapentin, and phenobarbital (Buell et al.). Tolerance to alcohol can also result in cross-tolerance to benzodiazepines and to a lesser degree barbiturates. Benzodiazepines and phenobarbital are positive allosteric modulators of GABA, and phenobarbital also blocks glutamate signaling. However, the main benefit of phenobarbital is that in down-regulation of GABA-A receptors alpha subunits that occurs in chronic alcohol use, benzodiazepines cannot bind, whereas phenobarbital binds directly to the ion channel and can function without the GABA-A receptors alpha subunit. Phenobarbital can be used as a monotherapy or in combination with benzodiazepines to treat alcohol withdrawal (Hawa et al.).

REBEL Cast Ep115 – Phenobarbital vs Lorazepam in Alcohol WithdrawalClick here for Direct Download of the Podcast

Clinical question: Is a phenobarbital-based or lorazepam-based alcohol detoxification protocol associated with a lower hospital length of stay compared to Ativan for alcohol withdrawal?

Paper: Hawa F et al. Phenobarbital Versus Lorazepam for Management of Alcohol Withdrawal Syndrome: A Retrospective Cohort Study. Cureus. 2021. PMID: 33728215

What They Did:* Retrospective cohort study (n=606) of patients admitted to three hospitals in Michigan for alcohol withdrawal between 2016 and 2018

Inclusion Criteria:* Aged 18-100 years * Admitted for alcohol intoxication or withdrawal treated with a CIWA-AR driven protocol * CIWA-AR = Clinical Institute Withdrawal Assessment for Alcohol Scale, Revised

Exclusion Criteria:* Admitted directly to the ICU * Pregnant patients * Prisoners * Patients who were transferred * Patients who received an addiction medicine consultation

Primary Outcome:

• Hospital length of stay

Secondary Outcomes:* Alcohol-related 30-day readmission * All-cause 30-day readmission * 30-day emergency department visits * ICU transfers

Results:

| Lorazepam (n=543) | Phenobarbital (n=63) | Unadjusted p-value | Propensity-score adjusted p-value | | Initial CIWA Score (+/- SD) | 9.05 (5.87%) | 11.02 (7.54%) | 0.049 | 0.859 | | Maximum CIWA Score (+/- SD) | 15.90 (7.1%) | 26.29 (6.57%) | 0.666 | 0.290 | | Initial BAL (n, %): | 0.865 | 0.906 | | <10 | 133 (26.55%) | 15 (25.86%) | | 10-100 | 72 (14.37%) | 8 (13.79%) | | 101-200 | 63 (12.57%) | 6 (10.34%) | | 201-300 | 87 (17.37%) | 14 (24.14%) | | 301-400 | 95 (18.96%) | 9 (15.52%) | | >400 | 51 (10.18%) | 6 (10.34%) |

Table 1: Selected clinical characteristics with and without propensity scoring for demographic and clinical variables.

Overall, the group that received phenobarbital had a higher initial CIWA score than the group that received lorazepam. The group that received phenobarbital had a higher maximum CIWA score, but the difference was not significantly significant. The difference in initial blood-alcohol levels were not statistically significant between the groups.

The primary outcome, hospital length of stay, was significantly shorter both before and after propensity score adjustment for the phenobarbital group. The 30-day emergency department readmission rate and all-cause 30-day readmission were significantly lower only when adjusted for propensity scores.

| Lorazepam (n=543) | Phenobarbital (n=63) | Unadjusted p-value | Propensity-score adjusted p-value | | Alcohol-related 30-day readmission (n, %) | 65 (11.97%) | 6 (9.52%) | 0.715 | 0.045 | | All-cause 30-day readmission (n, %) | 77 (14.18%) | 7 (11.11%) | 0.635 | 0.020 | | 30-day emergency department visits (n, %) | 101 (18.6%) | 7 (11.11%) | 0.195 | 0.015 | | ICU transfers (n, %) | 38 (7.04%) | 2 (3.23%) | 0.416 | 0.114 | | LOS (Days +/-SD) | 3.66 (2.32) | 2.805 (1.26) | <0.001 | <0.001 |

Table 2: Primary and secondary outcomes with and without propensity scoring for demographic and clinical variables.

Strengths:* Although this was not a randomized controlled trial, propensity scoring was used to adjust for variables that may have influenced physician selection of a lorazepam or phenobarbital protocol. The authors appropriately intended for this study to be a pilot observational study and did not complete a prospective randomized controlled trial to test for non-inferiority due to sample size limitations. * A broad range of variables were included that potentially influences treatment decisions and/or outcomes. * The protocols used in the study were using symptom-driven medications. Although symptom-triggered protocols require experienced staff and close monitoring, in previous studies the outcomes are associated with lower benzodiazepine doses and shorter lengths of stay in the hospital (Sachdeva et al.).

Limitations:* More information would have been helpful regarding the statistical methods regarding propensity scores. The study only mentioned that propensity-score weighting was used instead of propensity-score matching (i.e., 1:1 matching using propensity score, which typically discards some patients who do not have matches) (Olmos et al.). * The group that received phenobarbital had a higher maximum CIWA score than the group that received lorazepam, which could mean that phenobarbital was not as effective as lorazepam, although this is potentially confounded by patients who were transferred to the ICU were excluded from the study. Although CIWA has subjective components, when a patient has a CIWA in the 20s ICU transfer should be considered. * The study only examined symptom-triggered phenobarbital based on CIWA-Ar scoring, and it is unclear if there was front-loading, as phenobarbital (and benzodiazepines) sometimes are administered. This is beyond the scope of the paper but has been examined in other literature (Rosensen et al.) * The protocol at this hospital system was that all patients admitted to the ICU were started on a phenobarbital protocol, so the unadjusted score could reflect that sicker patients were started on the phenobarbital protocol based on variables that were not measured in the analysis. * The study does not address crossover, i.e., did some patients fail benzodiazepine treatment while inpatient and then get started on phenobarbital? Phenobarbital is also used in practice as a benzodiazepine-sparing adjunct in treating alcohol withdrawal. * The study did not include emergency department treatment in categorizing the patients, e.g., was there any crossover between treatment in the emergency department and treatment after admission? * Hospital C had 0 patients in the phenobarbital group (58 in the lorazepam group), which leads to concern about selection bias, i.e., were all the patients who the physicians would have started on phenobarbital sent to the ICU and thus excluded from the study? * The protocols in the hospitals in the study included phenobarbital and lorazepam IV, p.o., and IM, and the physician was able to choose the method of administration. One of the main benefits of phenobarbital is the 30-minute peak serum concertation when administered IV.

Discussion* Two randomized clinical trials exist for emergency department patients at this time: * A randomized, double-blind, placebo-controlled trial of emergency department patients (n=102) with alcohol withdrawal in the emergency department were treated with a loading dose of 10mg/kg phenobarbital versus placebo (Rosenson et al.) resulted in decreased ICU admissions (8% in the phenobarbital loading group versus 25% in the placebo group). Both groups received symptom-triggered lorazepam per institutional protocol. This study differed in that the phenobarbital administration was administered in a symptom-triggered protocol as opposed to a bolus. * A randomized, blinded clinical trial (Hendey et al.) of symptom-triggered phenobarbital versus symptom-triggered lorazepam in the emergency department (n=44). The phenobarbital arm received 260mg IV followed by 130mg IV PRN with no medications if discharged, and the lorazepam arm received 2mg doses followed by a chlordiazepoxide (Librium) taper if discharged. There was found to be no significant difference in CIWA scores at 48 hours between the two groups (p=0.6). A potential benefit in the phenobarbital group is that no medications were prescribed at discharge. * This study evaluated phenobarbital in the setting of a symptom-triggered protocol. A symptom-triggered protocol has been demonstrated to have improved outcomes when compared to a fixed taper when using benzodiazepines for alcohol withdrawal. However, a potential downside of symptom-triggered phenobarbital is that phenobarbital is sometimes underdosed. Large randomized clinical trials are warranted to provide further information regarding phenobarbital as an adjunct to benzodiazepine symptom-triggered management, phenobarbital using a loading dose, and phenobarbital monotherapy, among other topics.

Authors’ Conclusion:“Phenobarbital may be a reasonable alternative to lorazepam in management of AWS patients admitted to general medical units. When taking into account the BZDs-related adverse events including oversedation, encephalopathy, agitation, and increased risk of rebound withdrawal symptoms, phenobarbital may represent a reasonable alternative with a potential for improved outcomes.”

Our Conclusion:Although not the subject of this study, across multiple medical conditions, lower hospital lengths of stay are associated with lower morbidity and mortality as well as lower healthcare costs. Hospital length of stay is an important metric to take into consideration when starting someone on a protocol for alcohol detoxification in the emergency department. This topic will need to be revisited pending an RCT being completed currently (Filewood et al.) on a loading dose of phenobarbital versus placebo in addition to symptom-triggered benzodiazepine treatment in both study arms.

Clinical Bottom Line: Consider phenobarbital when starting treatment for alcohol withdrawal for patients who meet admission criteria.

References:1. Hawa F, Gilbert L, Gilbert B, Hereford V, Hawa A, Al Hillan A, Weiner M, Albright J, Scheidel C, Al-Sous O. Phenobarbital Versus Lorazepam for Management of Alcohol Withdrawal Syndrome: A Retrospective Cohort Study. Cureus. 2021 Feb 11;13(2):e13282. doi: 10.7759/cureus.13282. PMID: 33728215. 2. Buell D, Filewod N, Ailon J, Burns KEA. Practice patterns in treating severe alcohol withdrawal: a multidisciplinary, survey. J Intensive Care Med. 2019;23: 885066619847119.31122170 3. Mo Y, Thomas MC, Karras GE Jr. Barbiturates for the treatment of alcohol withdrawal syndrome: A systematic review of clinical trials. J Crit Care. 2016 Apr;32:101-7. doi: 10.1016/j.jcrc.2015.11.022. Epub 2015 Dec 8. PMID: 26795441. 4. Filewod N, Hwang S, Turner CJ, Rizvi L, Gray S, Klaiman M, Buell D, Ailon J, Caudarella A, Ginocchio GF, Santos M, Sandhu G, Dewhurst N, Sequeira K, Burns KEA. Phenobarbital for the management of severe acute alcohol withdrawal (the PHENOMANAL trial): a pilot randomized controlled trial. Pilot Feasibility Stud. 2022 Jan 22;8(1):14. doi: 10.1186/s40814-021-00963-4. PMID: 35065662. 5. Sachdeva A, Chandra M, Deshpande SN. A comparative study of fixed tapering dose regimen versus symptom-triggered regimen of lorazepam for alcohol detoxification. Alcohol Alcohol. 2014 May-Jun;49(3):287-91. doi: 10.1093/alcalc/agt181. Epub 2014 Jan 8. PMID: 24407777. 6. Olmos, Antonio and Govindasamy, Priyalatha (2015) “A Practical Guide for Using Propensity Score Weighting in R,” Practical Assessment, Research, and Evaluation: Vol. 20, Article 13. https://doi.org/10.7275/jjtm-r398. 7. Rosenson J et al. Phenobarbital for Acute Alcohol Withdrawal: A Prospective Randomized Double-Blind Placebo-Controlled Study. J Emerg Med 2013. PMID: 22999778. 8. Hendey GW, Dery RA, Barnes RL, Snowden B, Mentler P. A prospective, randomized, trial of phenobarbital versus benzodiazepines for acute alcohol withdrawal. Am J Emerg Med. 2011 May;29(4):382-5. doi: 10.1016/j.ajem.2009.10.010. Epub 2010 Mar 25. PMID: 20825805.

For More on this Topic Checkout:

• EmCrit: “Alcohol withdrawal,” Josh Farkas
• Tox and Hound: “Fear and loathing in alcohol withdrawal,” Jeff Lapoint

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Take Home Points

1. AVNRT is a common tachydysrhythmia that results from a reentrant loop within the AV node.
2. Unstable patients with AVNRT should be considered for immediate synchronized electrical cardioversion.
3. Stable patients with AVNRT can have a trial of vagal maneuvers followed by chemical cardioversion with adenosine or verapamil and synchronized electrical cardioversion if that fails.
4. Serum troponins should not routinely be obtained.

REBEL Core Cast 98.0 – AVNRTClick here for Direct Download of the Podcast

Definition: A regular, narrow-complex rhythm with a ventricular rate that is typically > 160 bpm. Atrioventricular nodal reentrant tachycardia (AVNRT) results from the presence of a reentry circuit in the AV node. This circuit conducts down the bundle of His (resulting in a narrow QRS) and generates retrograde conduction into the atria (inverted P waves buried within the QRS).

AVNRT is also referred to as paroxysmal supraventricular tachycardia (PSVT) or simply supraventricular tachycardia (SVT). However, it is important to understand that SVT is an umbrella term that refers to all tachydysrhythmias that originate above the ventricles including atrial fibrillation and atrial flutter, for example. When describing a supraventricular tachycardia that is due to a re-entrant circuit in the AV node specifically, it is better to use the term AVNRT as opposed to SVT in order to avoid confusion.

Differential to Consider (for Regular, Narrow Complex Tachydysrhythmias)

1. Sinus Tachycardia
2. AVNRT
3. Orthodromic Atrioventricular Reentrant Tachycardia (AVRT)
4. Atrial Flutter with 2:1 block

Common EKG Findings

• Narrow-complex, regular rhythm with a rate that often exceeds the theoretical maximal heart rate (220 – age) for that patient.
• Rhythm strip (or monitor): The rhythm is exquisitely regular. Sinus tachycardia and atrial flutter will have some minor variation in rate while AVNRT will not.
• ST depressions are commonly seen in AVNRT and can be diffuse (see EKG 1). These depressions are often rate related and of unknown significance.

AVNRT – LITFLAVNRT – LITFL 2AVNRT with Aberrancy

• Although AVNRT typically has a narrow-complex, some patients may demonstrate a wide-complex if the patient has aberrant conduction (baseline right or left bundle branch block or rate related bundle branch block).
• It can be difficult to differentiate AVNRT with aberrancy from ventricular tachycardia (VT). A number of algorithms have been constructed for this purpose, including the Brugada criteria, but none are perfect. Amal Mattu’s ECG Blog has an excellent review of AVNRT vs. VT and REBEL EM reviews the sensitivity and specificity of various algorithms.
• When in doubt, regular, wide-complex tachydysrhythmias should be treated as VT as this is the safest approach. [cross link to vt post]

Immediate Management: The primary goal is to convert the patient back to sinus rhythm.

Basics: ABCs, IV, O2 and Cardiac Monitor

Directed Management

• Establish patient stability
  • Unstable: Evidence of end-organ (brain, heart) malperfusion or hypotension. This may manifest as altered mental status, severe lightheadedness, severe shortness of breath or chest pain.
  • If the patient is unstable, proceed directly to electrical cardioversion
  • If the patient is stable, you may pursue non-pharmacological therapy with vagal maneuvers, electrical cardioversion or chemical cardioversion
• Vagal Maneuvers
  • Definition: maneuvers that increase stimulation of the vagal nerve resulting in increased vagal tone breaking the reentrant circuit
  • Examples
    • Carotid massage
      • Massage of the carotid sinus at the angle of the mandible
      • Caution
        • Do not perform bilateral carotid massage as this can markedly decrease blood flow to the brain
        • This maneuver is relatively contraindicated in elderly patients or those in whom you hear a bruit over the carotid as there is a theoretical risk of breaking off a carotid artery plaque and causing a stroke.
    • Valsalva maneuvers
      • Have patient bear down as if they are having a bowel movement
      • Have patient blow as hard as they can into a straw
      • Syringe technique
      • Postural Modification
        • Success rate: 43% vs. 17% (standard Valsalva) (Appleboam 2015)
        • Details of technique found at the St. Emlyn’s blog
• Electrical Cardioversion
  • Synchronized cardioversion is indicated for unstable patients with AVNRT
  • Synchronized cardioversion can also be strongly considered in stable patients with AVNRT
  • Dose: 100-200 J
  • Perform procedural sedation and analgesia if the patient’s hemodynamics allow
• Chemical Cardioversion
  • Adenosine
    • A naturally occurring purine nucleoside
    • Causes abrupt slowing of all AV conduction (anterograde and retrograde)
    • Dose: 6 mg fast IV push. If unsuccessful, dose can be doubled to 12 mg
    • Onset of action: 5-20 seconds
    • Duration of effect: 30 – 40 seconds
    • Key Point: because of adenosine’s short half-life, it must be given through a proximal peripheral IV (antecubital or closer) and as a rapid IV push. An alternate administration approach can be found on ALiEM.
  • Verapamil (Non-dihydropyridine Calcium Channel Blocker)
    • Class IV antidysrhythmic agent that slow Ca2+ channels and thus, slow conduction at the AV node and suppresses the SA node.
    • Multiple studies comparing verapamil to adenosine demonstrate equal efficacy of either agent with verapamil causing more hypotension (Delaney 2011, Hood 1992)
    • Dose: 0.07 mg/kg (most studies gave 5 mg over 2-5 minutes). Dose can be repeated
    • Should not be given to pediatric patients as there are reports of profound hypotension and circulatory collapse
  • Cardiac troponin is commonly elevated in patients with AVNRT but is often not associated with coronary artery disease (Ben Yedder 2011, Carlberg 2011)

Disposition:

• Most adult patients with AVNRT can be discharged after termination of the tachydysrhythmia.
• Pediatric patients should be considered for admission and further cardiology evaluation.
• Patients with frequent recurrences should be sent to a electrophysiologist for follow up.

Take Home Points

1. AVNRT is a common tachydysrhythmia that results from a reentrant loop within the AV node.
2. Unstable patients with AVNRT should be considered for immediate synchronized electrical cardioversion.
3. Stable patients with AVNRT can have a trial of vagal maneuvers followed by chemical cardioversion with adenosine or verapamil and synchronized electrical cardioversion if that fails.

Resources

• REBEL EM: SVT with Aberrancy Versus VT
• Amal Mattu’s ECG Case of the Week: August 26th, 2013
• ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe
• Larry Mellick: Treating SVT with Adensoine
• ALiEM: Trick of the Trade: Combining Adenosine with the Flush

References

1. Brugada P et al. A new approach to the diagnosis of regular wide complex tachycardia. Circulation 1991; 83: 1649-59. PMID: 2022022
2. Appleboam A et al. Postural mdodification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised trial. Lancet 2015. PMID: 26314489
3. Delaney B, Loy J, Kelly AM. The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis. Eur J Emerg Med. 2011; 18(3): 148-52. PMID: 20926952
4. Hood MA, Smith WM. Adenosine versus verapamil in the treatment of supraventricular tachycardia: a randomized double-crossover trial. Am Heart J. 1992; 123(6):1543-9. PMID: 1595533
5. Ben Yedder N et al. Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Can J Cardiol 2011; 27(1): 105-9. PMID: 21329868
6. Carlberg DJ et al. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med 2011; 29(5): 545-8. PMID: 20825871
7. Yealy D, Kosowsky JM: Dysrhythmias, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 79: p 1034-63.

Post Created By: Anand Swaminathan MD, MPH

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Take Home Points:

• Assess patients with floaters or flashers for retinal or vitreous detachment. Rapid diagnosis and emergency referral improves outcomes of ophthalmologic interventions.
• CRAO is a stroke of the eye; patients should be considered for a complete stroke work up.

REBEL Core Cast 97.0 – Acute Vision Loss IIClick here for Direct Download of the Podcast

Definition: Decrease of visual acuity due to a non-traumatic cause. Transient vision loss defined as vision loss <24 hours. Persistent vision loss defined as loss of vision >24 hours. (Bagheri 2015).

Causes: There are multitude of causes of vision loss. This post focuses on the following pathologies:

• Glaucoma
• Giant Cell Arteritis
• Vitreous Detachment
• Retinal Detachment
• Central Retinal Vein Occlusion
• Central Retinal Artery Occlusion
• Amaurosis Fugax

Vitreous Detachment (Guluma 2018)

Definition: Separation between the posterior vitreous cortex and the internal limiting membrane (ILM) of the retina (which is the most external portion of the retina).

Background

• Risk factors – Increasing age, myopia (nearsightedness)
• Many older individuals have essentially asymptomatic vitreous detachments.
• Often occurs as the vitreous shrinks with increasing age, pulling away from the retina.

Symptoms

• Floaters > flashers
• No change in visual fields
• May have decreased visual acuity.

Signs

• Shafer’s sign (tobacco dust)
• May see a Weiss ring when the posterior vitreous (PV) detaches from the optic disc margin
• Visualization with ultrasound.

Emergency Department Management:

• Emergency ophthalmology consultation.
• Emergency surgical management indicated if concomitant retinal tear, vitreous hemorrhage, or retinal detachment.

Retinal Detachment (Hollands 2009)

Pathophysiology

• Posterior vitreous shrinks with advancing age (aka synchysis senilis), pulling on the retina.
• Pulling can cause tears in the retina (10-15% of the time) (Hollands 2009)
• Tear allows liquefied vitreous leaks in, causing the retina to separate from the retinal pigment epithelium (33-46% of the time) (Hollands 2009)

Symptoms

• Blurry vision/decreased peripheral vision
• Flashers(photopsia)/floaters
  • 14% of pts referred to ophthalmology with flashers/floaters end up having retinal tears.
  • Photopsia is from vitreoretinal traction, floaters are from vitreous cells/blood in the eye.
  • Symptom characteristics (Hollands 2009)
    • Any flashers/floaters: (+) LR 1.2 and (–) LR 0.9.

    • 10 floaters, (+) LR 8.1-36

Signs

• Pigmented cells (‘‘tobacco dust’’ aka Shafer’s sign) in the vitreous and occasionally in the anterior chamber (caused by pigmented epithelial cells that spilled into vitreous)
• Visual field loss
• Vitreous hemorrhage: (+) LR 10
• Visualization on ultrasound

Emergency Department Management

• Emergency ophthalmology consultation for possible surgical repair

Central Retinal Vein Occlusion (CRVO) (McAllister 2012)

Background

• Pathophysiology not fully understood; possibly due to thrombus located in the central retinal vein (CRV), in the region of the lamina cribrosa
• Second most common cause of vision loss due to retinal vascular disease (Most common cause: Diabetic retinopathy)

Symptoms

• Floaters – CRVO can cause neovascularization which causes leaky vessels leading to debris in vitreous.
• Blurry vision
• Glaucoma symptoms – due to leaky vessels.
• May be asymptomatic

Signs

• Visual acuity deficit – Variable degree.
• Funduscopic exam-
  • Flame-shaped, dot and blot hemorrhages
  • Retinal edema: May be limited to a certain section of the retina (if branch occlusion) or in all quadrants (if central vein occluded) (aka pizza pie eye)
  • May have macular edema

Emergency Department Management

• Ophthomology consultation
• Treatment traditionally laser for neovascularization complications, although newer treatments are emerging.

Central Retinal Artery Occlusion (CRAO)

Background

• • Anatomy: First branch of the internal carotid artery is the ophthalmic artery which splits into the posterior ciliary and central retinal arteries which supply the eye.
  • Causes:
    • Carotid artery stenosis (most common)
    • Cardioembolic sources also important cause.

Symptoms

• Sudden painless monocular vision loss
• May have some temporal sparing.

Signs

• APD in affected eye
• Funduscopic exam: Whitening of ischemic inner retinal layers with sparing in the foveal region (which is supplied by the intact choroidal circulation) creating the classic “cherry-red spot”

Emergency Department Management

• Emergency ophthalmology consult, stroke work-up
• Treatment options:
  • No clinical trials have demonstrated improvement with any treatment compared with observation.
  • Management options described in the literature
    • Tissue plasminogen activator (tPA)
    • Ocular massage
    • Ocular pressure lowering agents / maneuvers
    • Topical agents such as timolol
    • IV agents such as acetazolamide or mannitol
    • Anterior chamber paracentesis
    • Vasodilatory Agents (nitroglycerin, pentoxifylline, isosorbide, carbogen, breathing into a bag – causes increase in CO2 leading to vasodilation)

Read More

Bhatia K, Sharma R: Eye Emergencies in Adams J.G. et al, Emergency Medicine Clinical Essentials ed 2. Philadelphia: Elsevier, 2013 (Ch) 26: p. 209-225

Walker R, Adhikari S.: Eye Emergencies, in Tintinalli J et al (eds): Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition New York City: McGraw-Hill 2016 (Ch) 241

Guluma K, Lee JE. Ophthalmology, in Marx J et al (eds): Rosens Emergency Medicine: Concepts and Practice, ed 9. Philadelphia: Elsevier, 2018 (Ch) 61: p. 790-819

Core Ultrasound: Vitreous vs Retinal Detachment

Post Created By: Anand Swaminathan MD, MPH

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Background: Historically, we have treated acute coronary syndrome with supplemental oxygen regardless of the patient’s oxygen saturation. This intervention was based on the belief that pushing the patient’s PaO2 to supra therapeutic levels would increase O2 delivery to ischemic myocardium and help reduce myocardial injury. More recent evidence, however, demonstrates that too much oxygen could be harmful (AVOID Trial) by causing coronary vasoconstriction and increasing oxidative stress.

The DETO2X-AMI trial (Link is HERE) was a randomized trial of patients with suspected acute myocardial infarction and showed no difference in one year mortality in patients given 12 hours of high flow O2 compared with limited O2. Based on recent studies, current guidelines recommend that O2 should not be given to non-hypoxemic patients with STEMI or NSTEMI [2,3].

REBEL Cast Ep114 – High Flow O2, Suspected ACS, and Mortality?Click here for Direct Download of the Podcast

Paper: Stewart, RAH et al. High Flow Oxygen and Risk of Mortality in Patients with a Suspected Acute Coronary Syndrome: Pragmatic, Cluster Randomised, Crossover Trial. BMJ 2021. PMID: 33653685

Clinical Question: Is there an association between high flow supplementary oxygen and 30-day mortality in patients presenting with a suspected acute coronary syndrome (ACS)?

What They Did: * Pragmatic, cluster randomized, crossover trial performed in 4 regions in New Zealand * The four geographical regions were randomly allocated to each of two oxygen protocols in six-month blocks over 2 years + High O2 protocol: Recommended O2 at 6 to 8L/min by face mask or 4L/min by nasal cannula for ischemic symptoms or EKG changes, irrespective of oxygen saturation (SpO2) + Low O2protocol: Recommended oxygen only if SpO2 was less than 90%, with a target SpO2 of <95%

Outcomes:* Primary: 30d all-cause mortality * Pre-Specified Secondary Outcomes: + 1-year all-cause mortality + Length of hospital stay

Inclusion:* Patients presenting with suspected ACS * Patients presenting to the ambulances and hospitals in the ANZACS-QI or ambulance ACS registries * Presenting during the defined study periods over 2 years

Exclusion:* None stated in the manuscript

Results:* 40,872 patients with suspected or confirmed ACS were included in the All New Zealand Acute Coronary Syndrome Quality Improvement registry or ambulance ACS pathway + 20,304 patients managed using high oxygen protocol + 20,568 patients were managed using low oxygen protocol * 10% had STEMI, 25% had NSTEMI, and 8% had unstable angina 30d * Mortality: + High O2 protocol: 3.0% + Low O2 protocol: 3.1% + aOR 0.96, 95% CI 0.86 to 1.08 * 4159 patients (10% of total population) had STEMI + 30d Mortality: + High O2 protocol: 8.8% + Low O2 protocol: 10.6% + aOR 0.78; 95% CI 0.63 to 0.97 * 10,218 patients (25% of total population) had NSTEMI + High O2 protocol: 3.6% + Low O2 protocol: 3.5% + OR 1.02; 95% CI 0.83 to 1.27

Strengths:* Groups were equally balanced in terms of baseline characteristics * Asks a clinically important question

Limitations: There were a significant number of protocol violations in a randomly selected group of patients that were audited * It is unclear what treatments outside of oxygen were given to either group * Low statistical power for a modest (0.6% absolute difference in all cause 30d mortality) effect of oxygen is a major limitation of this trial * Very little granular detail on treatments given to both groups, reinfarction rates, hospital admission for heart failure, troponin levels, or echocardiographic outcomes * Protocol non-adherence could have biased results toward no difference and decreased statistical power of the trial* * The duration of oxygen use was not documented, and it is unclear if one group received oxygen for a longer duration of time than the other

Discussion:* Groups were destined to look alike because neither had an intervention in most cases. Of the charts that were audited, most did not get O2. Does this study even achieve what it intended to? + When looking at final diagnosis of patients over 50% of patients in both groups had either a non-ACS condition or were not classified. The fact that >50% of patients had a non-ACS condition could explain the findings of no increase or decrease in 30d mortality. Why would patients without an ACS condition be included in a study that is evaluating the use of oxygen in ACS? + Another reason there is no surprise to the fact that this study didn’t show a difference in 30d mortality is simply looking at the SpO2 achieved: 98% in the high O2 group vs 96% in the low O2 group. Essentially there was no difference, meaning we wouldn’t expect to find a difference in outcomes + Although not patient oriented, why is there no breakdown of how many patients had cardiogenic shock, congestive heart failure, echocardiographic findings, or even troponin levels. Although death is a hard objective outcome, there are other outcomes worth knowing the results of and do impact patients quality of life * There does appear to be a small trend toward better outcomes in the STEMI cohort of patients with high O2 protocol compared to the low O2 protocol (8.8% vs 10.%) that was barely statistically significant. However, this was not the primary outcome of this trial and no definitive conclusions can be drawn. This is essentially a hypothesis generating outcome

Author Conclusion: “In a large patient cohort presenting with suspected ACS, high flow oxygen was not associated with an increase or decrease in 30 day mortality.”

Clinical Take Home Point: Unfortunately, this is a completely flawed trial that did not achieve any difference in SpO2 between groups (98% vs 96%), included >50% of patients without ACS, and had no granular details (troponin levels, echo findings, quality of life, treatments given between groups). Until further better evidence is produced, I recommend continuing to not use oxygen in patients with ACS who are normoxemic.

For More Thoughts on This Topic Checkout: REBEL EM: The DETO2X Trial: Do Patients with AMI Need Supplemental O2? * REBEL EM: The Death of MONA in ACS – Part II – Oxygen * REBEL Cast:* Ep13 – The AVOID Trial & The FLORALI Trial

References:1. Stewart, RAH et al. High Flow Oxygen and Risk of Mortality in Patients with a Suspected Acute Coronary Syndrome: Pragmatic, Cluster Randomised, Crossover Trial. BMJ 2021. PMID: 33653685 2. Amsterdam EA et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014. PMID: 25260718 3. Ibanez B et al. 2017 ESC Guidelines for the Management of Acute Myocardial Infarction in Patients Presenting with ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J 2018. PMID: 28886621 Post Peer Reviewed By: Anand Swaminathan, MD (Twitter: @EMSwami)

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Take Home Points:

• Suspect glaucoma in any patient with an acute change in vision and get an intraocular pressure measurement
• First line treatment in acute angle closure glaucoma is a topical beta blocker
• Consider giant cell arteritis in patients with unilateral headache, jaw claudication and change in vision
• Don’t wait for the biopsy to start steroids in giant cell arteritis as this therapy is vision saving

REBEL Core Cast 96.0 – Acute Vision Loss IClick here for Direct Download of the Podcast

Definition: Decrease of visual acuity due to a non-traumatic cause. Transient vision loss defined as vision loss <24 hours. Persistent vision loss defined as loss of vision >24 hours. (Bagheri 2015).

Causes: There are multitude of causes of vision loss. This post focuses on the following pathologies:

• Glaucoma
• Giant Cell Arteritis
• Vitreous Detachment
• Retinal Detachment
• Central Retinal Vein Occlusion
• Central Retinal Artery Occlusion
• Amaurosis Fugax

Glaucoma (Weinreb 2014, Schmidl 2015)

Definition: A group of diseases that have increased intraocular pressure (IOP), causing damage the optic nerve leading to decreased vision.

| Open angle | Closed angle | | Definitions | Increased resistance to aqueous outflow through the trabecular meshwork. | Access to the drainage pathways is obstructed | | Pathophysiology | Increase in IOP; Exact etiology unclear, but has a normal appearing anterior chamber angle and raised intraocular pressure (IOP). Asymptomatic until late in disease after vision loss occurs. Most common type of glaucoma | Occurs with obstruction to aqueous outflow, usually from the iris. Most common cause: pupillary block. | | Symptoms | Generally painless, asymptomatic. May have blurred vision or decreased visual acuity. | Painful vision loss, classically when going into a dark room. Other symptoms include halos around lights, nausea and vomiting. | | Signs | IOP >21. Decreased visual acuity, Cup to disc ratio >0.6 (difficult to see due to corneal edema) | IOP >21 (often >60), conjunctival injection, corneal edema, pupil that is hazy, fixed, mid-dilated. Cup to disc ratio >0.6 (difficult to see due to corneal edema) |

Emergency Department Management

• • All patients should get emergency ophthalmologic consultation
  • Start with eye drops (see table below) and add systemic medications if severe or refractory symptoms/IOP.
  • 1st line med: Timolol (beta blocker)
  • Topical meds can be given simultaneously except for pilocarpine, which is given after IOP is < 40 mmHg.

| Drug | Class | Dose | Mechanism | Side effects | | Timolol 0.5% | Beta blocker | 1 gtt | Reduces production of aqueous humor via decreasing cAMP concentration in the ciliary body | Can cause systemic effects, so if the patient has any contraindication to beta blocker, don’t use it. (contraindications = asthma, chronic obstructive pulmonary disorder, and patients with second and third degree heart blocks) | | Apraclonidine 1% | Alpha agonist | 1-2 gtt | Reduces production of aqueous humor plus increases outflow via contraction of the ciliary body | CNS effects and respiratory arrest in young children; caution in patients with cerebral or coronary insufficiency, postural hypotension, and renal or hepatic failure | | Pilocarpine 1-2% | Cholinergic | 1 gtt Q15 mins until IOP <40Given after Timolol | Causes iris to contract (miosis), which opens the canal more. Also can contract smooth muscle cells in the ciliary body, leading to an increase in aqueous outflow by widening the trabecular mechwork and Schlemm’s canal | Ciliary spasm leading to headaches in young patientsIneffective at IOP >40 mmHg | | Latanoprost | Prostaglandin | 1 gtt | Increase drainage through the uveoscleral outflow path. | Minimal systemic adverse effects; may be related to headaches | | Acetazolamide | Carbonic anhydrase inhibitor | 500 mg IV/PO | Reduces production of aqueous humor (CA makes bicarb, which is a major component of the aqueous humor) | Topical form has minimal systemic adverse effects; oral form may be associated with paresthesia, nausea, diarrhea, loss of appetite and taste, lassitude, or renal stones.Caution in sickle cell patients. | | Mannitol | Hyperosmotic agent | 1-2 grams/Kg IV | Reduces production of aqueous humor. | To minimize cerebral effects, and typically reserved if topical medications and acetazolamide do not work within 1 hour (from Rosens) |

Pro Tip: Can decrease systemic absorption of topical drops by putting pressure over medial surface of eye (over lacrimal duct) while placing drops.

Giant Cell Arteritis (arteritic anterior ischemic neuropathy) (Bagheri 2015, Hayreh 2009)

Pathophysiology

• Giant cell arteritis(GCA) affects that medium-sized and large arteries.
• T-cell-dependent disease.
• Predilection to involve the posterior ciliary artery. If not treated promptly, can cause profound bilateral visual loss without expeditious systemic corticosteroid treatment

Symptoms

• Often present with systemic symptoms, including anorexia and weight loss, malaise, myalgias
• Jaw claudication (can have tongue claudication as well)
• Headache (⅔ have this as primary symptom)
• Scalp tenderness
• Abnormal temporal artery and neck pain, myalgia, malaise and anemia.
• Transient unilateral vision loss (amaurosis fugax)
• Eye itself is usually painless.

Signs

• Decreased visual acuity common, but normal visual acuity does not rule out disease.
• Funduscopic exam:
  • Classic finding is a pale ‘‘chalky white” swollen optic nerve head (70% of patients) (Hyreh 1998)
  • Relative APD.

Lab tests

• Erythrocyte sedimentation rate (ESR).
  • Typically will see marked elevation.
  • A normal ESR does not rule out GCA
• C-reactive protein (CRP): CRP is the more sensitive marker for GCA
• Get both, because a positive ESR and CRP is close to 100% specific (Hayreh 2009)
• Gold standard test: temporal artery biopsy

Emergency Department Management:

• Ophthalmology/rheumatology consultation
• Prednisone: 80-100 mg Q24
  • Ideally, start steroids after biopsy performed
  • If high suspicion, start empiric steroids as unlikely to markedly alter biopsy results
  • Duration of steroids (Hayreh 2009)
    • Until the CRP and ESR go back down to normal
    • Often takes 2-3 weeks.
    • Followed by a steroid taper

Take Home Points

• Suspect glaucoma in any patient with an acute change in vision and get an intraocular pressure measurement
• First line treatment in acute angle closure glaucoma is a topical beta blocker
• Consider giant cell arteritis in patients with unilateral headache, jaw claudication and change in vision
• Don’t wait for the biopsy to start steroids in giant cell arteritis as this therapy is vision saving

Read More

Bhatia K, Sharma R: Eye Emergencies in Adams J.G. et al, Emergency Medicine Clinical Essentials ed 2. Philadelphia: Elsevier, 2013 (Ch) 26: p. 209-225

Walker R, Adhikari S.: Eye Emergencies, in Tintinalli J et al (eds): Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition New York City: McGraw-Hill 2016 (Ch) 241

Guluma K, Lee JE. Ophthalmology, in Marx J et al (eds): Rosens Emergency Medicine: Concepts and Practice, ed 9. Philadelphia: Elsevier, 2018 (Ch) 61: p. 790-819

EM docs: Central Retinal Artery Occlusion

CanadiEM: Medical Concepts – Acute Angle Closure Glaucoma

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Take Home Points:

• Fluorescein is an essential tool in the diagnosis of HSV keratitis
• Identifying the type of HSV keratitis is crucial, as it will guide treatment
• Update tetanus vaccination
• Consult ophthalmology if there is concern for HSV keratitis as these patients require close and frequent follow-up

REBEL Core Cast 95.0 – Herpetic KeratitisClick here for Direct Download of the Podcast

Definition: An infection of the cornea caused by the herpes simplex virus (HSV).

Epidemiology:

• Most frequent cause of corneal blindness in the United States
• Most common source of infectious blindness in the Western world. Approximately 2 million people worldwide have impaired vision from herpetic eye disease (Farooq 2012)

Pathophysiology:

• Primary infection: occurs most commonly in the mucocutaneous or ocular distribution of the trigeminal nerve, and can present as a non-specific upper respiratory infection
• Latency: the virus spreads from the infected epithelial cells to the cell body in the trigeminal ganglion where the virus persists indefinitely in a latent state
• Reactivation: interneuronal spread of HSV within the ganglion allows patients to develop subsequent ocular disease without ever having had primary ocular HSV infection
• HSV keratitis can be divided into 3 types: epithelial, stromal, and endothelial (White 2014)
  • Epithelial: caused by actively replicating virus and occurs in the outermost layer of the cornea
  • Stromal: caused by immune mechanisms and occurs in deeper layers
  • Endothelial: caused by chronic inflammation and occurs in deeper layers
• Sequelae:Recurrent HSV keratitis can cause corneal scarring, ulceration, and perforation, ultimately leading to astigmatism and permanent vision loss.

Clinical Exam:

Symptoms:

• Eye pain
• Corneal injection
• Visual changes (blurry vision, decreased visual acuity)
• Tearing
• Discharge
• Photophobia

Physical exam:

• Visual acuity should be performed in all patients
• Fluorescein staining
  • May reveal dendritic lesions (linear branching patterns with terminal bulbs)
  • If the lesion enlarges, it can form a geographic ulcer
• Slit lamp exam
  • Used to identify disease in deeper (stromal + endothelial) layers
  • Stromal disease shows up primarily as an inflammatory infiltrate with stromal edema, vascularization, and scarring

Diagnostics:

• The diagnosis of HSV keratitis is based on clinical eye exam.
• In the absence of dendritic lesions, decreased corneal sensation should increase concern for herpetic keratitsis (Weiner 2013)
• Viral culture
  • Gold standard test
  • Impractical in the ED: expensive, delayed
• Ophthalmology may perform additional testing, such as viral culture/PCR and Tzanck smear, to confirm the diagnosis but these are not routinely recommended (Welder 2012)
• Pitfalls: these tests are only positive when live virus is present, and cannot be used to diagnose stromal keratitis (White 2014)

Management:

• Most cases of HSV epithelial keratitis resolve spontaneously within 3 weeks. However, the American Academy of Ophthalmology recommends treatment of epithelial keratitis to prevent recurrence and progression to stromal or endothelial keratitis.
• Epithelial keratitis:
  • Trifluridine 1% solution: 1 drop Q2hours for 7 days OR
  • Ganciclovir 0.15% gel: five times per day
  • Oral antiviral agents (not FDA approved, but equal efficacy in studies) (Wilhelmus 2010)
  • Corneal debridement
• Stromal and endothelial keratitis:
  • Urgent referral to ophthalmology
  • Topical corticosteroid
  • Oral antiviral agents for 10 weeks as prophylaxis reduces the rate of recurrent herpetic keratitis (Wilhelmus 1999)

Take Home Points:

• Fluorescein is an essential tool in the diagnosis of HSV keratitis
• Identifying the type of HSV keratitis is crucial, as it will guide treatment
• Update tetanus vaccination
• Consult ophthalmology if there is concern for HSV keratitis as these patients require close and frequent follow-up

References:

Farooq AV et al. Herpes simplex epithelial and stromal keratitis: an epidemiologic update. Surv Ophthalmol 2012; 57(5):448-462. PMID: 3652623

Wilhelmus KR et al. Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis. Cochrane Database Syst Rev 2010; (12): CD002898. PMID: 4739528

Weiner et al. Demystifying the ocular herpes simplex virus. American Academy of Ophthalmology. Link

McDonald et al. Management of epithelial herpetic keratitis: an evidence based algorithm. Link

Welder et al. Herpes simplex keratitis. University of Iowa Health Care. Link

Wilhelmus KR et al. Herpetic Eye Disease Study. A controlled trial of topical corticosteroids for herpes simplex stromal keratitis. Ophthamology 1999; 101(12):1883-1896. PMID: 7997324

Chan RV et al. Herpes simplex keratitis – Latin America. American Academy of Ophthalmology. Link

White et al. Herpes simplex keratitis: A treatment guideline – 2014. Link

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Take Home Points

• SBO should be considered in all patients presenting with abdominal pain particularly if they have a prior abdominal surgical history
• Patients with SBO often have non-specific signs and symptoms. There is no history or physical exam feature that rules out the disease
• Lactate elevation is a late finding in SBO. A normal lactate does not rule out the diagnosis
• Plain X-rays perform poorly in making or ruling out the diagnosis. CT is the most widely accepted imaging modality but US (both formal and ED) has better performance characteristics
• Patients with SBO should have an emergent surgical consultation and treatment should start with good supportive care (IV fluids, electrolyte repletion, antiemetics)
• Patients with hypotension, hypoperfusion or frank sepsis from an SBO should be aggressively resuscitated and optimized for operative management

REBEL Core Cast 94.0 – SBOClick here for Direct Download of the Podcast

Definition: Obstruction of the intestines such that bowel contents are unable to pass through the small bowel into the large bowel

• Mechanical Obstruction: presence of a physical barrier to the passage of bowel contents.
  • • Examples: adhesions, neoplasms, inflammatory disease (i.e. Crohn’s), hernias, intussusception, parasitic infections and foreign bodies
    • Simple Obstruction: Obstruction occurs at a single point in the bowel
    • Closed-loop obstruction: Obstruction at two locations creating a segment of bowel with proximal and distal compromise of blood flow
• Functional (neurogenic) Obstruction: Obstruction resulting from disruption of normal peristalsis in the GI tract in the absence of a mechanical obstruction (adynamic ileus). Examples include post-operative, hypokalemia and opiate use

Pathophysiology

• Dilation of the bowel proximal to the obstruction
  • Results in accumulation of intestinal secretions and partially digested materials
  • Stimulates peristalsis resulting in early loose bowel movements as well as nausea and vomiting
• Bowel wall becomes edematous
  • Decreased absorption capacity leading to further dilation
  • Decreased venous return and, ultimately, decreased arterial flow
• Bacterial overgrowth occurs as a result of stasis
• Translocation of bacteria (notably E.Coli) into the bloodstream can occur due to increased bowel wall permeability
• Extensive fluid losses can result from transudative fluid loss into the bowel lumen
• Recurrent vomiting can lead to metabolic alkalosis, electrolyte abnormalities and hypovolemia
• Closed Loop Pathophysiology
  • Intraluminal pressure increases more rapidly due to inability of bowel contents to move in retrograde fashion
  • Venous and arterial compromise can occur more rapidly leading to intestinal ischemia and infarction
  • Infarction and necrosis of the bowel can lead to perforation with resulting peritonitis and sepsis

Abdominal XRay with Air Fluid LevelsPresentation (Taylor 2013)

• History
  • Abdominal pain
    • Often crampy in nature
    • Crescendo-decrescendo pattern
  • Abdominal distension
  • Nausea/Vomiting (more pronounced with proximal obstructions)
  • Constipation
  • Obstipation (inability to pass gas- typically a late finding)
  • Prior abdominal surgery or radiation treatments common
• Physical Examination
  • Early findings
    • Generalized tenderness to palpation
    • Decreased bowel sounds or high pitched “tinkling”
      • (+) LR Abnormal Bowel Sounds: 6.33
      • (-) LR Abnormal Bowel Sounds: 0.27
  • Late findings
    • Fever
    • Abdominal distension
      • (+) LR: 5.64 – 16.8
      • (-) LR: 0.34 – 0.43
    • Absent bowel sounds
    • Peritoneal signs (i.e. rebound and guarding)

Diagnostics

• Laboratory Tests
  • Commonly ordered lab tests (i.e. WBC) are non-sensitive and non-specific
  • Serum lactate
    • Elevated in cases of bowel ischemia or infarction
    • Elevation typically a late finding
• Abdominal X-ray
  • Findings
    • Dilated loops of small bowel proximal to the obstruction
    • Visible valvulae conniventes (mucosal folds of the small intestine)
    • Air-fluid levels
    • String-of-beads sign (small pockets of gas within a fluid-filled small bowel)
  • Advantages: Rapidly performed, non-invasive, can be performed bedside in unstable patients
  • Disadvantages: Poor sensitivity and specificity
  • Test Characteristics (Taylor 2013)
    • (+) LR: 1.6 (1.1 – 2.5)
    • (-) LR: 0.43 (0.24 – 0.79)

• CT Scan with Fluid Filled, Dilated Loops of BowelCT Scan

  • Findings
    • Dilated loops of small bowel > 2.5 – 3 cm (measure outer wall to outer wall)
    • Collapsed loops of bowel distal to the obstruction
    • Intestinal Ischemia/Infarction
      • Thickened bowel wall
      • Increased attenuation of the bowel wall
      • Pneumatosis intestinalis (non-specific)
      • Portal venous gas (non-specific)
  • Advantages
    • Increased sensitivity and specificity to plain radiographs
    • Often identifies cause of obstruction
    • Can identify alternate pathology or cause of symptoms
  • Disadvantages
    • Takes more time
    • Requires patient to leave department (may not be feasible if patient unstable)
  • Test Characteristics (5 – 10 mm slice) (Taylor 2013)
    • (+) LR: 3.6 (2.3 – 5.4)
    • (-) LR: 0.18 (0.09 – 0.35)
  • Ultrasound
  • Findings
    • Dilated loops of bowel (diameter > 2.5 cm) – most sensitive and specific
    • Decreased peristalsis and retrograde peristalsis (to and fro sign or “whirling”)
    • Bowel Infarction/Ischemia
      • Fluid filled bowel with extra-luminal free air
      • Bowel wall thickening (> 3 mm)
      • Absence of peristalsis

  • US With Dilated Loops of BowelAdvantages

    • Non-invasive
    • Can be rapidly performed at the patient’s bedside
    • Excellent test characteristics
      • Disadvantages
    • Dependent on operator skill
    • Patient habitus may limit quality of images
    • Does not clearly delineate transition point
    • May not be accepted by consulting services for definitive diagnosis
      • Test Characteristics (Taylor 2013)
    • Formal US
      • (+) LR: 14.1 (3.6 – 55.6)
      • (-) LR: 0.13 (0.08 – 0.20)
    • ED US
      • (+) LR: 9.5 (2.1 – 42.2)
      • (-) LR: 0.04 (0.01 – 0.13)

SBO

Immediate Management:

Basics:

• Airway
  • It is uncommon for patients with SBO to have airway compromise
  • Patients with closed-loop obstruction can become septic and obtunded while having continued vomiting
• Circulation
  • Advanced cases can develop septic shock
  • Most cases will have intravascular volume depletion secondary to transudation of fluids into the bowel and decreased PO intake
  • Volume expansion with isotonic fluids (Lactated ringers, 0.9% saline or balanced solutions) indicated
• Electrolyte repletion as necessary (fluid loss will be accompanied by electrolyte loss)
• Antiemetics: may be helpful in those with partial SBO and in those not actively vomiting

Directed Management

• Surgical Consultation
  • Surgical exploration indicated (Maung 2012)
    • Patients with evidence of clinical deterioration
    • Patients with generalized peritonitis
    • CT findings with bowel ischemia or infarction
  • Non-operative patients will require serial abdominal examinations and consideration for operative management if the clinical picture changes
• Nasogastric Tube (NGT) Placement
  • Traditional teaching argues for the use of NGT in all patients with SBO but literature to defend this approach is minimal (Paradis 2014)
  • Resolution of nausea/vomiting with antiemetics may obviate the need for an NGT
  • Indications for NGT placement
    • Intractable vomiting
    • Severe abdominal distension
    • Altered mental status or other aspiration risk
• Antibiotics
  • Theory is that bacterial translocation from the gut will be increased due to bowel wall edema
  • Limited data to support administration in all cases (Maung 2012)
  • Broad-spectrum antibiotics should be administered in patients with signs of hypoperfusion and sepsis
• Disposition
  • All patients should be admitted to a surgical service
    • Limited evidence demonstrates lower mortality and better outcomes in SBO admitted to surgical service (Oyasiji 2010)
    • Patients more likely to get operative intervention earlier upon decompensation
  • Patients with closed loop obstructions or signs of ischemia/infarction should be admitted to an ICU setting

Take Home Points

1. SBO should be considered in all patients presenting with abdominal pain particularly if they have a prior abdominal surgical history
2. Patients with SBO often have non-specific signs and symptoms. There is no history or physical exam feature that rules out the disease
3. Lactate elevation is a late finding in SBO. A normal lactate does not rule out the diagnosis
4. Plain X-rays perform poorly in making or ruling out the diagnosis. CT is the most widely accepted imaging modality but US (both formal and ED) has better performance characteristics
5. Patients with SBO should have an emergent surgical consultation and treatment should start with good supportive care (IV fluids, electrolyte repletion, antiemetics)
6. Patients with hypotension, hypoperfusion or frank sepsis from an SBO should be aggressively resuscitated and optimized for operative management

Read More

• The Short Coat: Small Bowel Obstruction – A Likely Story?
• Radiopaedia: Small Bowel Obstruction
• 5 Min Sono: SBO
• Ultrasound Podcast: Episode 36 – Small Bowel Obstruction
• LITFL: Small Bowel Obstruction
• FOAMCast: Episode 23 – SBO and Mesenteric Ischemia
• Roline CE, Reardon RF: Disorders of the small intestine, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 92: p 1216-1227.

References

1. Taylor MR, Lalani N. Adult small bowel obstruction. Acad Emerg Med 2013; 20(6): 528-44. PMID: 23758299
2. Maung AA et al. Evaluation and management of small-bowel obstruction: an eastern association for the surgery of trauma practice management guideline. J Trauma Acute Care Surg 2012; 73(5): S362-9. PMID: 23114494
3. Paradis M. Towards evidence-based Emergency Medicine: Best BETs From the Manchester Royal Infirmary. BET 1: Is Routine Nasogastric Decompression Indicated in Small Bowel Occlusion? Emery Med J 2014; 31(3): 248-9. PMID: 24532357
4. Oyasiji T et al. Small bowel obstruction: Outcome and cost implications of admitting service. Am Surg 2010; 76:687-691. PMID: 20698371
5. Images
6. Air Fluid Levels: Case courtesy of Dr Aditya Shetty, Radiopaedia.org. From the case rID: 28737
7. CT SBO Case courtesy of Dr Jeremy Jones, Radiopaedia.org. From the case rID: 6135
8. US SBO Case courtesy of Dr Maryam Saif AlAli, Radiopaedia.org. From the case rID: 43438

| Sensitivity | Specificity | (+) LR | (-) LR | | Decr Bowel Sounds (or high pitched “tinkling) | 23 – 76% | 88 – 93% | 3.29 – 6.33 | 0.27 – 0.83 | | Abdominal Distension | 62 – 67% | 89 – 96% | 5.64 – 16.8 | 0.34 – 0.43 | | Abdominal X-ray | 75% | 66% | 1.6 | 0.43 | | CT Scan | 87% | 81% | 3.6 | 0.18 | | Radiology US | 90% | 96% | 14.1 | 0.13 | | ED US | 97%% | 90%% | 9.5 | 0.04 |

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Take Home Points

• Lithium toxicity comes in a three flavors: acute, chronic and acute on chronic. Each form will have a different presentation as well as management.
• Lithium levels are often unreliable in terms of guiding management and must be taken in context with symptoms and time of ingestion (in acute overdose).
• IV fluids are a cornerstone of management as increasing intravascular volume and increasing renal elimination are critical.
• Hemodialysis is indicated for a lithium level > 5 mEq/L or a level > 4 mEq/L in a patient with renal failure. However, dialysis decisions should be made in conjunction with a toxicologist.

REBEL Core Cast 93.0 – Lithium ToxicityClick here for Direct Download of the Podcast

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Take Home Points

• Perichondritis is an infection of the cartilage and connective tissue of the ear
• Perichondritis can be recognized clinically by erythema, swelling and tenderness of the auricle.
• The most common organism in perichondritis is P. aeruginosa and antibiotics should be tailored to cover this organism

REBEL Core Cast 92.0 – PerichondritisClick here for Direct Download of the Podcast

Background

1. Perichondritis may appear to be a simple cellulitis of the ear but, in fact, it represents an infection of the connective tissue of the ear.
2. Misdiagnosis and mistreatment of perichondritis is common and can lead to significant morbidity

Critical Point #1: Perichondritis is an infection of the cartilage and connective tissue of the ear

• Perichondritis often appears as simple cellulitis but, the infection goes much deeper.
• Abscess and cavitation of the cartilage is common

Critical Point #2: Perichondritis can be recognized clinically by erythema, swelling and tenderness of the auricle.

• Over time, this may progress to severe otalgia and purulent discharge
• The lobule is often spared as is the external canal

Critical Point #3: The most common organism in perichondritis is P. aeruginosa and antibiotics should be tailored to cover this organism

• Typical cellulitis treatment with cephalexin, TMP-SMX or doxycycline will not treat this disorder
• Fluoroquinolones (I.e. ciprofloxacin) can be used as first line therapy but some patients will fail this treatment due to increasing resistance and require parenteral antibiotics

Left: Cellulitis
Right: PerichondritisReferences

Noel, Stella Boustany, et al. “Treatment of Pseudomonas aeruginosa auricular perichondritis with oral ciprofloxacin.” The Journal of dermatologic surgery and oncology. 15.6 (1989): 633-637. (PMID: 2723226)

Kullar, Peter, and Philip D. Yates. “Infections and foreign bodies in ENT.” Surgery (Oxford) 30.11 (2012): 590-596. (PMID: 27057069)

Caruso, Andria M., Macario Camacho Jr, and Scott Brietzke. “Recurrent auricular perichondritis in a child as the initial manifestation of insulin-dependent diabetes mellitus: A case report.” ENT: Ear, Nose & Throat Journal 93.2 (2014). (PMID: 24526489)

REBEL EM: Perichondritis

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Take Home Points Methemoglobinemia can result from exposure to a number of different medications. The most common are dapsone and topical anesthetic agents (i.e. benzocaine) Consider the diagnosis in any patient with cyanosis and hypoxia that doesn’t respond to oxygen administration Administer methylene blue to any patient with abnormal vital signs, metabolic acidosis, end organ ... Read more

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Take Home Points Spontaneous Bacterial Peritonitis (SBP) is a difficult diagnosis to make because presentations are variable. Consider a diagnostic paracentesis in all patients presenting to the ED with ascites from cirrhosis An ascites PMN count > 250 cells/mm3 is diagnostic of SBP but treatment should be considered in any patient with ascites and abdominal ... Read more

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Take Home Points Severe hypocalcemia can cause hypotension and QTc prolongation leading to Torsades de Pointes.  Treat moderate to severe symptoms and any EKG changes with IV calcium salts Always search for and treat the underlying cause of hypocalcemia REBEL Core Cast 88.0 – Hypocalcemia Click here for Direct Download of the Podcast Definition: A ... Read more

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Take Home Points Patients with severe hypercalcemia (> 14 mg/dL) are at risk for severe cardiac dysrhythmias and cardiac collapse Treatment centers on volume repletion with normal saline with consideration for the addition of loop diuretics AFTER volume reexpansion is complete As the patient begins to diurese, continually monitor electrolytes REBEL Core Cast 87.0 – ... Read more

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REBEL Core Cast 86.0 – Hand Nerve Blocks Click here for Direct Download of the Podcast References: Core Ultrasound: Median Nerve Block Core Ultrasound: Radial Nerve Block Core Ultrasound: Ulnar Nerve Block Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Background: Hypoxemia is a commonly encountered adverse event during rapid sequence intubation (RSI) in the ED. Critically ill patients in the ED often have a lack of physiologic reserve, decreased cardiac output, increased shunting, and reduced pulmonary reserves. Therefore, a strategy that safely avoids desaturation and prolongs safe apnea times would be beneficial. There are ... Read more

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Background: Some of the feared complications of endotracheal intubation include hypotension, cardiac arrest, and death (cardiovascular collapse). These complications can result from numerous causes including medication-induced vasodilation and decreased venous return to the heart due to increased intrathoracic pressure from positive pressure ventilation. In recent years there has been an increased focus on resuscitation prior ... Read more

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Take Home Points SVT >5cm or <3 cm from the SFJ should be treated with anti-coagulation.  The rate of concurrent DVT and PE in patients with SVT is 25% and 5%, respectively.  REBEL Core Cast 85.0 – Superficial Venous Thrombosis Click here for Direct Download of the Podcast Definition: The presence of a clot in ... Read more

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Take Home Points AVNRT is a common tachydysrhythmia that results from a reentrant loop within the AV node. Unstable patients with AVNRT should be considered for immediate synchronized electrical cardioversion. Stable patients with AVNRT can have a trial of vagal maneuvers followed by chemical cardioversion with adenosine or verapamil and synchronized electrical cardioversion if that ... Read more

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Take Home Points Post dural-puncture headache affects up to 30% of patients after lumbar puncture. Suspect PDPH in all patients who recently underwent an LP or epidural anesthesia regardless of whether they meet the IHS criteria. The best way to treat PDPH is to prevent it from developing. Techniques proven to reduce risk include large ... Read more

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Background: Early in the COVID-19 pandemic, clinicians were looking for practical, widely available, and low-cost interventions to help patients with hypoxemia. One of those interventions was awake prone positioning. Potential mechanisms of benefit in awake proning include more uniform distribution of tidal volume, recruitment of areas in the posterior part of the lung, improved ventilation/perfusion, ... Read more

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Take Home Points Consider AAA in patients with acute onset of back or abdominal pain particularly in patients > 50 and in those with a history of hypertension Consider ruptured AAA in patients (especially those > 50 years of age) with unexplained hypotension, back or abdominal pain All ruptured AAAs should be considered unstable regardless ... Read more

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Take Home Points Emergency medicine revolves around the differential diagnosis History and physical exam should significantly narrow your differential diagnosis Have an idea of what specific diagnoses are being ruled out when ordering diagnostic tests Always consider the most life-threatening and most common disease processes first – we are a rule out specialty “Red flags” are ... Read more

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Take Home Points Emergency medicine revolves around the differential diagnosis History and physical exam should significantly narrow your differential diagnosis Have an idea of what specific diagnoses are being ruled out when ordering diagnostic tests Always consider the most life-threatening and most common disease processes first – we are a rule out specialty “Red flags” are ... Read more

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Take Home Points Break the differentials down into bad & painless, bad & painful, and other causes – WOMAN-PE Cardiac causes – mechanical or electrical – look for the obvious and 5 non-obvious causes (WPW, HCOM, ARVD, prolonged QT, and Brugada) Ask the red flag questions – was there a prodrome, signs of seizure activity ... Read more

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Take Home Points Be prepared to do everything with these cases, if they can’t provide information, dive into their medication list, history, contact whoever you have to to get more information Keep differentials wide – then approach these cases with the mindset of focal vs generalized weakness and work from there Focal – ask about ... Read more

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Take Home Points Key point is to discern between central and peripheral causes – become familiar with the nuances of one and concentrate on that Assume central and convince yourself its peripheral in nature, if at the end of the evaluation, you can’t do that, assume a central cause and do a work-up Using timing ... Read more

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Take Home Points Examine all parts of the body, even inside the mouth – this can be the difference between benign and life threatening rashes Truly emergent causes: meningococcemia, TTP, DIC, TSS, SJS, TEN, and necrotizing fasciitis Toxic appearing patients with petechia/purpura = sepsis until proven otherwise Look for medication reactions: Sulfa, Penicillins, NSAID’s, ABX, ... Read more

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Take Home Points Look for the red flags – hypotension, environmental exposures, medications (SS, NMS), SIRS/qSOFA criteria Be on the lookout for neutropenic fever – isolate patients, administer abx early, and admit Sepsis definition is changing all the time – be aware of current guidelines Remove pre-existing indwelling lines/catheters in the setting of sepsis – ... Read more

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Take Home Points Sprains need more support than just an ace wrap – place them in an aircast or a splint Perform a thorough physical exam – take off their shoes and socks Lisfranc and Maisonneuve injuries are often missed – make sure to exam the bottom of the foot for echymosis, eval for mid ... Read more

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Take Home Points Approach leg pain with the seconds, minutes, hours mindset – think about acute limb ischemia, compartment syndrome, and necrotizing fasciitis Do a thorough physical exam – get their shoes and socks off – you will find crazy stuff when you actually look Palpate and image the joint above and below any injury ... Read more

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Take Home Points Don’t make bite width to small – look at the curvature of the needle – start the bite at half the curvature of the needle Don’t pull too tight – this will pucker the skin and lead to poor healing due to ischemia at the wound borders Laceration repairs are not sterile! ... Read more

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Take Home Points Ask about the red flags: cancer, fever, IVDA, FND, point tenderness, saddle/perianal anesthesia, trauma, urinary retention, bowel incontinence, weight loss Most don’t need XR’s – set this expectation and advise against bed rest Consider XR’s: h/o cancer, extremes of age, osteoporosis, new back pain in the elderly, trauma Perform POCUS and check ... Read more

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Take Home Points Get a upreg on any childbearing age female with vaginal bleeding – this is an ectopic pregnancy until proven otherwise Confirm vaginal vs rectal bleeding – it can be hard for patients to tell, especially the elderly Quantify the amount of blood loss – soaking thru >1 pad/hr is a lot Ask ... Read more

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Take Home Points Get a upreg on every female patient of child bearing age with lower abdominal pain – this is an ectopic pregnancy until proven otherwise Always consider ovarian/testicular pathology for lower abdominal pain Always have a chaperone when performing genitourinary physical exams Ovarian cysts >5 cm are at high risk for torsion, consider ... Read more

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Take Home Points Diffuse abdominal pain can be anything – keep a broad differential and work from there Old patient and flank pain = aortic catastrophe – aortic dissections and aneurysms can knock off flow to the kidneys Appendicitis and diverticulitis can presents diffusely early in their clinical presentation before they localize Kidney stones are ... Read more

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Take Home Points Patients don’t necessarily know what’s important – ask lots of questions, find out if they’ve been taking a ton of NSAID’s or Tylenol for their pain and now they have an ulcer or hepatitis Keep a broad differential – the kidneys, the aorta, and consider chest pain differentials in any patient with ... Read more

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Take Home Points Go in thinking sick vs not sick – this can take time to develop and that’s ok, this skill will come as you see more patients If you’re thinking about getting a scan or u/s – just get it! You don’t want to go home thinking you should have gotten a scan ... Read more

The post REBEL Core Cast – Basics of EM – Introduction to Abdominal Pain appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points Think about causes – is it the head, the belly, or something else leading to the vomiting Get a upreg on all females of childbearing age Peritoneal signs – look for rebound/guarding, consider surgery consult prior to imaging if unstable Ask about last BM and if their passing gas – avoid metoclopramide ... Read more

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Take Home Points Take chest pain seriously – ACS and PE patients don’t always appear ill – look for the silent killer cases Remember 4-2-1 approach to chest pain = 4 chambers, 2 lungs, 1 esophagus EKG’s – get an old one to compare to for every patient and make sure to perform serial EKG’s Concerning ... Read more

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Take Home Points Wheezing can be absent when severe – be wary of the silent chest = impending respiratory failure Not everything that wheezes is asthma! Beware of mimics – COPD, CHF, anaphylaxis, stridor Consider dexamethasone in those with poor compliance – has equal efficacy to prednisone Refill all meds prior to discharge MDI with ... Read more

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Take Home Points Keep a wide differential Think of the airway, lungs, heart, blood, kidneys, acid/base, brain Use Wells & PERC consecutively to stratify those who you think may have a PE Silent chest is asthma patients is a harbinger of impending airway compromise Use ultrasound for every respiratory complaint Treat early and aggressively to ... Read more

The post REBEL Core Cast – Basics of EM – Shortness of Breath appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points Constantly evolving disease with various presentations Identify those that are hypoxic are deliver appropriate oxygen therapy Give steroids to those that are hypoxic Educate patients about the course of the disease and what to look out for the requires hospitalization Encourage vaccination! REBEL Core Cast – Basics of EM – COVID-19 Click ... Read more

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Take Home Points Be aware of the red flags – fever, HIV, hemoptysis, TB risk factors Is the onset acute or chronic Characterize sputum production – spoon full, cup full, bucket full- Hemoptysis – most can have streaking and thats normal with bronchitis Always fall back on your H&P – your dx will be in ... Read more

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Take Home Points Look for the red flags – fever, drooling, neck stiffness, toxic ingestion, uvula deviation, voice changes Steroids help with swelling Obtain CT soft tissue neck for concerning presentations Don’t be a cowboy/cowgirl – get consultants involved early – ENT/Anes/OMFS Make sure you repeat vital signs prior to discharge – if patient remains ... Read more

The post REBEL Core Cast – Basics of EM – Sore Throat appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Message Do not ignore abnormal vital signs – they can be the harbinger of badness Watch out for developing withdrawal, treat early and aggressively These patients are a major fall risk – keep rails up, place on safety observation Obtain a CT Head for anyone with external signs of trauma EtOH level not ... Read more

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Take Home Points Walk in – decide sick/not sick Do I need help now? If so, call in the troops Stable – start asking questions – A LOT OF THEM Investigate – reach out to family, bystanders, EMS, PMD, pharmacy Perform a head to toe exam – check the jiblets and scan the bladder for ... Read more

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Take Home Points Always check the vital signs of the eye – visual acuities, field of vision, ocular pressure Go in thinking whether you have to call Optho or not Get the story – was there trauma or did it just appear? Do the exam – Is it red or painful, are there changes in ... Read more

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Take Home Points Patients >65 or suspected of intoxication are at high risk for bleeds – scan them!! Epidural has a lucent period – be wary of decompensation and perform frequent re-evals. Anti-coagulated patients must be reversed. FFP takes hours to work, PCC takes minutes. Nasal fractures – examine septum for hematoma – need to ... Read more

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Take Home Points Hypertension rarely causes headache, it’s usually the other way around. Patients with headaches are in pain, and in turn, may have elevated blood pressures. Treat the underlying issue and you’ll treat the HTN at the same time. Get a pregnancy test on all female patients – you don’t want to miss a ... Read more

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REBEL Core Cast – Basics of Emergency Medicine Podcast Welcome to the EMRA Basics of Emergency Medicine Podcast. I am your host EJ Wright, and the following series is an all encompassing approach to the most common chief complaints in the ED based on the well known EMRA Basics of Emergency Medicine, A Chief Complaint-Based ... Read more

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Take Home Points Priapism is compartment syndrome of the penis. Ischemia and infarction can occur with prolonged priapism and rapid treatment and detumescence is critical Provide adequate analgesia early to facilitate necessary interventions. Dorsal block of the penis is the most effective analgesic approach Do not delay aspiration and irrigation if more conservative measures fail ... Read more

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Background: Currently, trauma resuscitation focuses on immediate hemorrhage control, resuscitation with blood products (i.e. PRBCs, plasma) and early administration of tranexamic acid. The evidence for the use of blood-based resuscitation in the pre-hospital system has been mixed (PAMPer and COMBAT trials). While early administration of blood products makes physiologic sense, proof of benefit is important ... Read more

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Take Home Points Compartment syndrome is a life and limb threatening emergency that requires early recognition, prompt diagnosis and immediate management with fasciotomy While clinical evaluation is flawed, pain out of proportion to injury and pain with passive stretch of muscles within the compartment are the best screening tools. Do not wait for the development ... Read more

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Bottom Line: Based on the limited available evidence, it’s unlikely orthostatic vital sign measurement can be used to determine which patients have volume loss and which do not. The baseline prevalence of orthostatic vital signs is common and patients will not always develop orthostatic vital signs in response to volume loss. Therefore, there will both ... Read more

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In this episode of the REBEL Cast Book Club, Swami, Marco, Steve, and Brandon discuss how the lessons learned from Col. Chris Hadfield’s “An Astronaut’s Guide to Life on Earth” might apply to emergency medicine. REBEL Reflections Episode 3: An Astronaut’s Guide To Life on Earth Click here for Direct Download of the Podcast Post ... Read more

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Take Home Points Classically, herpes zoster will present with rash and pain in a dermatomal distribution Immunocompromised patients are at greater risk for significant complications of zoster, including visceral dissemination and zoster ophthalmicus Appropriate therapy includes antiviral therapy within 72 hours of onset of symptoms and analgesia for acute neuritis Disseminated zoster and zoster ophthalmicus ... Read more

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Take Home Points Think about flexor tenosynovitis in a patient with atraumatic finger pain. They may have any combination of these signs: Tenderness along the course of the flexor tendon Symmetrical swelling of the finger – often called the sausage digit Pain on passive extension of the finger and Patient holds the finger in a ... Read more

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Background: In the past few years there has been a growing debate between the use of balanced multielectrolyte solutions (BMES) and saline in the critically ill (See the “for more about this topic” section below). Recent research has yielded inconsistent results with RCTs showing improved mortality (SMART), no change in mortality (BaSICS), and decreased acute ... Read more

The post REBEL Cast Ep108: The PLUS Trial – Balanced vs Unbalanced Fluids in the Critically Ill appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Core Cast 76.0 – Zoom Better Click here for Direct Download of the Podcast Read More P Cubed Presentations: Zoom, Zoom, Zoom P Cubed Presentations: Online Presentation Setup P Cubed Presentations: How To Do An Online Presentation YouTube Tutorials: Link is HERE Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Take Home Points: Newer data suggests that the infection and DVT rates for femoral lines are similar to that for internal jugular central lines. In a resuscitation situation, there are likely faster ways to obtain access than a femoral line (ie IO, Peripheral IV). If you are going to place a femoral line, use ultrasound ... Read more

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Background: Emergency endotracheal intubation is a potentially life-saving procedure in the management of critically-ill patients. The inherent risks associated with the procedure challenge us to refine our skills and adopt new techniques that can improve our performance. The bougie is an inexpensive device that has gained considerable traction in the last ten years. In 2018, ... Read more

The post REBEL Cast Ep107: The BOUGIE Trial – Bougie First in All Emergency Intubations? appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points: Cauda equina syndrome is a rare emergency with devastating consequences Early recognition is paramount as the presence of bladder dysfunction portends bad functional outcomes The presence of bilateral lower extremity weakness or sensory changes should alert clinicians to the diagnosis. Saddle anesthesia (or change in sensation) and any bladder/bowel changes in function ... Read more

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Mechanical Ventilation is a modality commonly used in the critically ill, but many providers, may not have a strong understanding of the basics. Emergency Medicine and Critical Care Physicians need to have a firm grasp of the basic concepts of mechanical ventilation because without it, we can do serious harm to our patients. Airway management ... Read more

The post REBEL Crit Cast Ep6.0 – Mastering Mechanical Ventilation Part 1 appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points: First line treatment for asthma exacerbations is inhaled beta agonists, inhaled anticholinergics and systemic corticosteroids. The majority of patients presenting to the ED with asthma exacerbations should be started on short-burst corticosteroids to control inflammation and prevent admission and relapse. Diagnostic testing is not required for the majority of patients with asthma ... Read more

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Take Home Points: Lung ultrasound is simple, quick and accurate for real time, bedside assessment of your patient with acute undifferentiated dyspnea PTX: least dependent area, shallow depth, lung sliding, lung point CHF: scan across the 4 zones of the chest, look for B lines Bringing this to the bedside can give you diagnostic closure ... Read more

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Background: The utility of pharmacological interventions for patients with OHCA are rather limited with no robust evidence that they improve outcomes. Calcium, one of the pharmacological options has both inotropic and vasopressor effects. Additionally, calcium plays an important role in the management of hyperkalemia which is a significant cause of cardiac arrest. There have been ... Read more

The post REBEL Cast Ep106: The COCA Trial – Calcium in Cardiac Arrest appeared first on REBEL EM - Emergency Medicine Blog.

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In this episode of REBEL Cast, Anand Swaminathan and I sit down to discuss the utility of thrombolysis prior to Endovascular therapy for LVO acute ischemic stroke. The discussion is broken up into two potential scenarios: Not all facilities are comprehensive stroke centers In comprehensive stroke center, time from door to groin puncture will be ... Read more

The post REBEL Cast Ep 105: Thrombolysis Before Endovascular Therapy for LVO Acute Ischemic Stroke appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points: DOPES is not just a memory tool. It give you a structured approach to taking care of vented patients with vital sign changes. Check for dislodgement of the tube, obstruction of the tube, pneumothorax, equipment failure, breath stacking and dyssynchrony. Don’t forget that the patient can have more than one issue; always ... Read more

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Take Home Points: Prioritize ABCs and systematic evaluation of the trauma patient with an open fracture as one third of these patients have multiple injuries Assess neurovascular status and immediately reduce and immobilize if compromised Give appropriate antibiotics as soon as possible Consult orthopedics for operative management as soon as possible REBEL Core Cast 70.0 ... Read more

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There are generally 3 main congenital heart diseases presentations that young children between ages of 0 days to about 3 months will present with. Often times you will see experts split these congenital heart lesions into 2 categories: Cyanotic vs Acyanotic lesions. Either is an acceptable approach as long as you split the acyanotic lesions ... Read more

The post REBEL Crit Cast Ep5.0 – Conquering Congenital Cardiac Lesions appeared first on REBEL EM - Emergency Medicine Blog.

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Background: Two prior trials compared the addition of vasopressin 20 IU (for each dose of epinephrine) and methylprednisolone 40mg to placebo for in hospital cardiac arrest. The 1st trial was published in 2009 [2] and the second in 2013 [3]. In the 2009 study, the combination of vasopressin-epinephrine and methylprednisolone improved survival. In the 2013 ... Read more

The post REBEL Cast Ep104: VAM-IHCA – Vasopressin and Methylprednisolone for In-Hospital Cardiac Arrest appeared first on REBEL EM - Emergency Medicine Blog.

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Take home points: Epiglottitis has demonstrated a resurgence in the adult population. It is no longer a pediatric only disease. The classic presentation of epiglottitis (3Ds of drooling, dysphagia and distress) is uncommon Epiglottitis should be high on your differential for the bounce-back patient who continues to complain of worsening sore throat Definitive diagnosis is ... Read more

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I was fortunate enough to record a podcast on Rob Orman’s, Stimulus podcast on Oct 14th, 2021. We both felt it was an important enough topic that we should post it on both his and my site. The treatment of non-hospitalized patients suffering from COVID-19 is a hot topic and constantly changing. In this podcast ... Read more

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Take-Home Points Always consider STEMI as the diagnosis prior to diagnosing pericarditis. If the EKG shows convex ST elevations, reciprocal ST depressions, or dynamic changes, the patient is much more likely to have a STEMI. Patients with pericarditis should be treated with a combination of NSAID/Aspirin and Colchicine Patients with large pericardial effusions, tachycardia out ... Read more

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Background information: Buprenorphine and buprenorphine-containing medications are being used in emergency departments for treatment of patients with opioid use disorder (1). Buprenorphine is a high-affinity partial agonist of the μ-opioid receptor. Buprenorphine has a higher affinity for the μ-opioid receptor than full agonists such as heroin, oxycodone, fentanyl, and methadone. Thus, if a patient is ... Read more

The post REBEL Cast Ep102: High-Dose Buprenorphine Induction in the Emergency Department for Treatment of Opioid Use Disorder appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Cast Book Club Episode 2: The New Jim Crow   Click here for Direct Download of Podcast Post Peer Reviewed By: Anand Swaminathan, MD (Twitter: @EMSwami) and Salim R. Rezaie, MD (Twitter: @srrezaie)

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The reviewed article highlights the complex relationships between six themes: Improving the processing of information Promoting effortful learning Applying learned information to new and varied contexts Developing expertise Harnessing the power of emotion for learning Teaching and learning in a social context. REBEL Core Cast 67.0 – Tips for Medical Education Click here for Direct ... Read more

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Take Home Points Once you figure out the neonate that presented to your ED is sick, run through a differential of why then can be sick so you don’t anchor. I like to use TIMOT (Trauma, Infection, Metabolic, Organs, Tox) but use whatever works for you. Use your detailed history looking for risk factors to ... Read more

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Background: The clinical importance of immediate coronary angiography after out of hospital cardiac arrest (OHCA) without STEMI continues to be debated. A systematic review and meta-analysis published in 2016 suggested that this set of patients has a high likelihood of having a culprit lesion when getting a catheterization. However, the studies included in this review ... Read more

The post REBEL Cast Ep101: The TOMAHAWK Trial – Angiography after OHCA without STEMI appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL Core Cast 65.0 – Idiopathic Intracranial Hypertension Click here for Direct Download of Podcast Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Take Home Points Pancreatitis is diagnosed by a combination of clinical features (epigastric pain with radiation to back, nausea/vomiting etc) and diagnostic tests (lipase 3x normal, CT scan) A RUQ US should be performed looking for gallstones as this finding significantly alters management The focus of management is on supportive care. IV fluids, while central ... Read more

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Take Home Points Adrenal insufficiency is a life-threatening emergency; recognize early and treat aggressively Hallmark is hypotension refractory to IVF/pressors Suspect in patients with unexplained hypotension and risk factors Prior glucocorticoid therapy History of autoimmune diseases Hyperpigmentation AIDS or TB history Treat empirically with hydrocortisone 100mg IV and search for precipitating causes Less than 50% ... Read more

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Background: COVID-19 is now a vaccine preventable illness but, unfortunately, many have not received the COVID-19 vaccine due to a number of reasons including access, misinformation and a lack of confidence. In the US, the emergency department is the safety net of healthcare and could play a bigger role in increasing vaccination rates in vulnerable ... Read more

The post REBEL Cast Ep100: REVVED UP – COVID-19 Vaccination in the ED appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points Infuse factor first, investigate later Treat when bleeding is suspected, not confirmed. Have a low threshold! It is better to over treat than undertreat. Give full dose when in doubt Factor 8 = 50U/kg Factor 9 = 100 U/kg Beware of hidden bleeds (brain, retroperitoneal, deep muscles) If patient has inhibitors, or ... Read more

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Take Home Points 1. Debriefing is critical. Studies show numerous benefits in terms of team communication and staff ability to regroup. 2. Start by gathering your team, thanking them for their work and noting that nothing could have changed the patient’s ultimate outcome. 3. Summarize the events so everyone is on the same page and ... Read more

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Take Home Points – Unexplained tachycardia (or any abnormal vital sign) warrants investigation. – Pain, induration, “woody” feel of any muscle group should raise suspicion of infection in that muscle group that has spread hematogenously especially in those with predisposing factors (e.g HIV, trauma, IVDA) – Early pyomyositis will not necessarily have abscess formation – ... Read more

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Take Home Points Neck movement (both extension and flexion) has the ability to cause cord damage. Using hyperangulated blade in video laryngoscopy improves chances for glottic visualization in patients with a c-collar in place. Ultimately, hypoxemia kills – Intubate the patient with what you have available, as there has not been shown to be a ... Read more

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REBEL Core Cast 58.0 – Wound Care IV Click here for Direct Download of Podcast Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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REBEL Core Cast 58.0 – Crush Your Rotation Click here for Direct Download of Podcast Read More EMRA: Making the Most of Patient Presentations Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Background: It’s no surprise that unplanned, emergency intubations are significantly different from intubations in the operating room (OR). Unplanned intubations on the floors and in the ED and ICU settings are highly unlikely to be “physiologically optimized:” they have underlying shock, respiratory failure, metabolic acidosis, as well as other pathophysiological changes that can substantially increase ... Read more

The post REBEL Cast Ep99: The INTUBE Study – Adverse Peri-Intubation Events in the Critically Ill appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points If youre concerned about a retained foreign body make sure to get imaging There is a higher risk of wound infection associated with age, diabetes, wound size, contamination, and a location not on the head or neck. Other conditions that impair wound healing include renal failure, obesity, malnutrition, immunocompromised status. Prophylactic antibiotics ... Read more

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Take-Home Points: The conditions needed to achieve flow are: Clear goals Immediate feedback Balance between challenge and skill We can use the flow state to supercharge our productivity. Establish clear goals Preform deep work Reflect on shortcomings REBEL MedEd Cast Ep1.0: – Autotelics and Flow Click Here for Direct Download of the Podcast Definition of ... Read more

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Take Home Points There is no strict golden hour for wound closure. Location, contamination and patient factors all should be taken into account Dog bites can be closed primarily. Bites on the hand and foot are higher risk for infection. If you close, strongly consider adding antibiotic prophylaxis Sterile water is unnecessary for wound decontamination ... Read more

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Background: It has long been thought that intravenous contrast can lead to acute kidney injury. Recent data, however, has called this dogmatic teaching into question. Unfortunately, the data arguing against the association of contrast with AKI comes from observational trials and, thus, carry with it numerous biases. One potential bias is baseline differences in the ... Read more

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Take Home Points FBs are a very common complication of wounds. X-ray is poor at detecting foreign bodies US is a tremendous tool and be used dynamically at the bedside to assist w FB extraction Prophylactic antibiotics are not routinely recommended REBEL Core Cast 54.0 – Wound Care I – Foreign Bodies Click here for ... Read more

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REBEL Cast Book Club Episode 1: The Coddling of the American Mind Click here for Direct Download of Podcast Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Take Home Points Altered mental status has numerous possible etiologies. Splitting it into vital sign issues, toxic/metabolic, infectious processes, CNS issues (bleed, mass) and psych/dementia is a good way to organize your thoughts Hypertensive encephalopathy is a diagnosis of exclusion – make sure you’re not dealing with another process like meningitis or an intracranial hemorrhage ... Read more

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Procrastination is simply put, a voluntary delay of tasks that we intend to do. In this REBEL Core Cast, Anand Swaminathan, MD and Marco Propersi, DO sit down and talk about why we procrastinate and steps we can each take to overcome it. REBEL Core Cast 52.0 – Procrastination Click here for Direct Download of ... Read more

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REBEL Core Cast 51.0 – Conference Pearls Click here for Direct Download of Podcast Read More REBEL EM: Epidural Abscess REBEL EM: Pacemaker Basics Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

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Background: Epistaxis is a common Emergency Department (ED) complaint with over 450,000 visits per year and a lifetime incidence of 60% (Gifford 2008, Pallin 2005). Standard anterior epistaxis treatment consists of holding pressure, use of local vasoconstrictors, topical application of silver nitrate and placement of an anterior nasal pack. ED patients with epistaxis often fail ... Read more

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Background: Opioid-related emergency department visits have been increasing over the past two decades in correlation with increasing rates of heroin use in the United States. Naloxone, which is used to reverse heroin overdose, has a half-life of approximately 60 to 90 minutes (2). A 4 to 6 hour observation period after naloxone reversal has typically ... Read more

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Take Home Points SVT >5cm or <3 cm from the SFJ should be treated with anti-coagulation. The rate of concurrent DVT and PE in patients with SVT is 25% and 5%, respectively. REBEL Core Cast 50.0 – Superficial Venous Thrombosis Click here for Direct Download of Podcast Definition: The presence of a clot in a ... Read more

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Background: Science by press release. Not the way any of us would choose to operate but, the COVID pandemic has made this a reality. It’s vital that we understand that while pharmaceutical companies have a responsibility to release this information, we as clinicians should not be practicing medicine based on press releases. Of course, these ... Read more

The post REBEL Cast Ep95: Colchicine in COVID (COLCORONA)? Don’t Believe the Hype. appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points Consider ruptured AAA in patients (especially those > 50 years of age) with unexplained hypotension, back or abdominal pain All ruptured AAAs should be considered unstable regardless of vital signs as rapid deterioration is common A ruptured AAA is 100% fatal without surgical or endovascular intervention. Mobilize your surgical colleagues early REBEL ... Read more

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Take Home Points Frostbite is a severe, localized cold-induced injury due to freezing and thawing of tissue. We usually see these injuries affecting the ears, nose, cheeks, chin, fingers, and toes. Patients will complain of cold, numb or stiff sensations and discoloration of the skin. Critical ED treatment starts with rewarming in a warm, ... Read more

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Take Home Points Nausea and Vomiting has an exceedingly large differential – don’t just anchor on GI presentations H&P important – Duration, frequency, content, and associated symptoms Alcohol swab -> If no line and want quick treatment give swab Ondansetron -> oral you can give without hesitation but if giving IV check QTC / electrolytes ... Read more

The post REBEL Core Cast 47.0 Nausea and Vomiting appeared first on REBEL EM - Emergency Medicine Blog.

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Background: Current trauma resuscitation prioritizes control of bleeding and uses massive transfusion protocols to prevent and treat coagulopathy. This is typically done in the form of massive transfusion protocols delivered in proportions that approach the composition of whole blood. Two strategies to help guide this replacement of blood products are conventional coagulation tests and viscoelastic ... Read more

The post REBEL Cast Ep94: The ITACTIC Trial – Viscoelastic Hemostatic Assay Augmented Protocols appeared first on REBEL EM - Emergency Medicine Blog.

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Back in April 2020, on REBEL Cast episode 79 we sat down to discuss COVID-19. Specifically, we focused on not intubating patients early and why ARDSnet may not be the best ventilator paradigm for patients with COVID-19. By popular demand, we decided to follow up on this podcast. We are now just about 9 months ... Read more

The post REBEL Cast Ep93: COVID-19 – A Follow Up on Not Intubating Early and ARDSnet appeared first on REBEL EM - Emergency Medicine Blog.

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Background: Intravenous alteplase is the current standard care for treatment of acute ischemic stroke (AIS) despite active debate on the research supporting its use. The window for its use has been restricted to <3h of symptom onset based on the results of the NINDS trial and extended to a time window of <4.5h based on ... Read more

The post REBEL Cast Ep92: Alteplase for Stroke of Unknown Time of Onset? appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points This is a resuscitative hysterotomy – focus is on saving the mother first. Delivering the fetus can improve venous return thus increasing chance to save mom Don’t focus on gestational age to make the decision – if you think the belly is big enough to be causing compression of vascular structures, the ... Read more

The post REBEL Core Cast 46.0 – Resuscitative Hysterotomy appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points Be sure to consider mesenteric ischemia in any elderly patient with abdominal pain or lower gastrointestinal (GI) complaints. Remember, the presentation can be tricky to find and they may have a reassuring abdominal exam. Ask about artherosclerotic risk factors, history of cardiovascular disease including atrial fibrillation and prior embolic events, and a ... Read more

The post REBEL Core Cast 45.0 – Mesenteric Ischemia appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points When approaching the patient with uspected seizure, focus on questions that matter in determining if the event was a seizure or not...

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Background: Acute gastrointestinal bleeding (GIB) is a common diagnosis dealt with by emergency clinicians.  Definitive therapy for acute GIB often includes endoscopy or surgery. However,...

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Take Home Points Heat stroke is a life-threatening disorder characterized by elevated core temperature, compromise to neurologic function and multi-system organ dysfunction The keystone of...

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Background: Here we go again with another “Time is Brain,” acute ischemic stroke study.  The authors start out by saying that earlier administration of intravenous...

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I am fortunate to work in a hospital system that is very forward thinking.  We have a phenomenal relationship with our intensivists, and I have...

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Take Home Points Small to Moderate Size Pneumothorax – consider managing conservatively with observation (need to make sure consulting services on same page) Needle aspiration...

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Background: Upper endoscopy allows for the identification of the source of bleeding as well as hemostatic treatment for actively bleeding lesions In patients with upper...

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Take Home Points Forget the “traditional” needle decompression landmark Decompress at 4th or 5th intercostal space in the anterior axillary line REBEL Core Cast 32.0...

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Goals of lung protective mechanical ventilation: Minimizing harm during mechanical ventilation with a lung-protective strategy with: Low tidal volume (TV) Limit plateau pressure to <30mmHg...

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Early reports have shown that COVID-19 is most likely causing a hypercoagulable state, however the prevalence of acute VTE and exactly how to treat it...

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In this episode of REBEL Cast,I sit down with Richard Levitan and talk about some ideas from his experience in New York, where he spent...

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Take Home Points N95 masks ideally should be single use but in COVID19 times, safe reuse practices are critical. The best approach to reuse is...

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Airway Pressure Release Ventilation (APRV) is a mode of ventilation that allows spontaneous breathing throughout the ventilation cycle.  It is a time-cycled mode of ventilation...

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Take Home Points Hyperthyroidism can present along a spectrum from the minimally symptomatic to severely decompensated and presentation can vary with age If there are...

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Hey there REBEL Cast listeners, Salim Rezaie here.  For me and I am sure many COVID-19 has been quite the whirlwind.  So much information, so...

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Background: Peripheral intravenous (PIV) access is one of the most commonly performed invasive procedures in unwell patients.  Although, most patients can have PIVs placed by...

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The American Heart Association (AHA) released a focused update in 2019, for advanced cardiovascular life support (ACLS) guidelines, to addend those published in 2017 and...

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Take-Home Points Before starting a neonatal resuscitation, take some deep breaths to calm yourself Call in your friends – get a second team to manage...

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Background: Vasopressors are often used to improve hypotension and perfusion in an effort to decrease mortality of patients with septic shock. Mean arterial pressure (MAP)...

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Vascular Disasters Take Home Points Consider vascular pathologies in all of your patients with atraumatic limb pain – especially those with typical and atypical risk...

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Take Home Points  No palpable pulse does not equal no perfusion. We aren’t great at feeling pulses Patients with moderate to severe signs and symptoms...

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Take-Home Points Endocarditis can have vague and varied presentations and has high morbidity and mortality. Be on the lookout in patients with risk factors including: ...

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The use of heated and humidified high flow nasal cannula (HFNC) has become increasingly popular in the treatment of patients with acute respiratory failure through...

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Take Home Points When compared to 0.9% saline, lactated ringers is a more balanced solution and more closely resembles our serum. SALT ED and SMART...

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Background: The combination of vitamin C, hydrocortisone and thiamine in sepsis has been a topic of hot debate in the past couple years.  There is...

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Take Home Points  Osteomyelitis is an infection in any part of a bone. It has a varied presentation including acute and chronic forms. Patients can...

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Therapeutic Hypothermia (also called targeted temperature management (TTM)) is a deliberate reduction of the core body temperature to 32 – 34°C, in patients who suffer...

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Background: Traditionally, vasopressors have been given through central venous catheters (CVCs) in the critically ill.However, the time it takes to place a CVC is time...

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REBEL EM-ers: Salim & I would like to introduce the launch of a new REBEL EM project. We are adding a podcast focused on a...

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Take Home Points Important as front line providers to know research and data behind stroke care Patients eligible for endovascular care are those with large...

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Take Home Points  Ask the patient if they vape! Worry about the sick looking patient and those seen recently CXR is nonspecific and CT might...

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Take Home Points    End stage liver disease patients have fragile baseline physiology. Minor insults can have profound effects Always start with the basics –...

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REBEL Core Cast 21.0 – ECG in Syncope Click here for Direct Download of Podcast Sample ECGs Post Peer Reviewed By: Salim R. Rezaie,...

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Take Home Points   Stress cardiomyopathy looks like ACS/STEMI, with patient presenting with chest pain, dyspnea or maybe syncope. It looks like ACS and should be...

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Background: Currently, alteplase is the mainstay of treatment of acute ischemic stroke.  Advocates of alteplase suggest that the benefit of alteplase is greatest when given early...

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Take Home Points  Acute closed angle glaucoma is an ophthalmologic emergency that usually presents with sudden, painful, monocular vision loss. Physical exam will reveal conjunctival...

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Take Home Points When looking at pH and bicarb, the differences between VBG and ABG are miniscule. For DKA patients, stick with the VBG as...

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Take Home Points: Get definitive airway control when necessary Use modality you’re most comfortable with Hard signs –  pulsatile bleeding, bruit or thrill, expanding hematoma,...

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Background: Convulsive status epilepticus is the most common pediatric neurological emergency worldwide.  Currently, phenytoin (UK & Europe) or fosphenytoin (USA) is the recommended second-line IV...

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Take Home Points Myxedema coma is severe, decompensated hypothyroidism with a very high mortality. Classic features include: decreased mental status, hypothermia, hypotension, bradycardia, hyponatremia, hypoglycemia,...

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Background: Antibiotics are one of the cornerstones of therapy in the treatment of sepsis/septic shock, however according to the Surviving Sepsis Campaign (SSC) guidelines, time to...

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Take Home Points There is no real distinction between syncope and near syncope. Older folk with near syncope or syncope should be treated the same....

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This is a special edition REBEL Cast done by my good friend Andy Little, DO (Twitter: @andylittle).  As I was busy running the 2nd annual...

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This is a special edition REBEL Cast done by my good friend Andy Little, DO (Twitter: @andylittle).  As I was busy running the 2nd annual...

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Take Home Points on SVT Superficial venous thrombosis refers to a clot and inflammation in the larger, or “axial” veins of the lower extremities and...

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Take Home Points on Measles There is a resurgence of measles worldwide Incubation period is 10 – 14 days and patients are contagious 4 days...

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Background: Despite the lack of replication of the NINDS & ECASS-3 trials, guidelines recommend the use of tPA in the ≤4.5hr window after the onset of...

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Take Home Points on Tracheostomy Emergencies Track is mature in 7 days – don’t blindly replace before then because concern for false track creation All...

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Take Home Points on Epiglottitis Epiglottitis has demonstrated a resurgence in the adult population. It is no longer a pediatric only disease. The classic presentation...