REBEL Cast

🧭 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. 📝 Introduction When 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 Management 1. Oxygenation — Getting O₂ InPrimary 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 OutPrimary 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 AcidosisRR ↑ to blow off CO₂ and buffer acidosis.ARDSTidal 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 Matters Ventilator 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 Resident Cape Fear Valley Internal Medicine Residency Program Fayetteville NC Aspiring Pulmonary Critical Care Fellow Showing Slide 1 of 1 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 143.0–Ventilators Part 3: Oxygenation & Ventilation — Mastering the Balance on the Ventilator appeared first on REBEL EM - Emergency Medicine Blog.

🧭 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. 📝 Introduction Mechanical 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 Line Understanding 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, MD Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Nicole Ebalo, DO Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Showing Slide 1 of 2 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 142.0–Ventilators Part 2: Simplifying Mechanical Ventilation – Most Common Ventilator Modes appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown Click here for Direct Download of the Podcast. ⏰ Highlights 00:00 Introduction to Rebel Cast00:10 Highlighting the Incrementum Conference 202600:34 Meet the Founders of Incrementum01:21 The Journey to Incrementum04:27 The Recognition of Emergency Medicine in Spain06:04 What is Incrementum?08:14 Bringing Together Top Emergency Medicine Experts11:38 Exciting Sessions to Look Forward To15:54 Conclusion and Invitation to Incrementum 2026 📝 Introduction In 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 DO All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Core Cast 146.0–Ventilators Part 4: Setting up the Ventilator Ventilator management can feel overwhelming—there are so many knobs to ... Thoracic and Respiratory Read More REBEL Core Cast 145.0: Understanding QTc Prolongation: Causes, Risks, and Management The QT interval is a vital part of ECG interpretation, ... Procedures and Skills Read More REBEL Core Cast 144.0: Tourniquet Tips In this episode of the Rebel Core Content podcast, Swami ... Procedures and Skills Read More REBEL Core Cast 138.0: A Simple Bedside Approach to Shock In this episode, we will dive into a simple yet ... Cardiovascular Read More REBEL Core Cast 131.0 – Traumatic Arthrotomy Take Home points: Always suspect an open joint if there ... Trauma Read More REBEL Core Cast 130.0 – Omphalitis Take Home Points Early diagnosis: erythema and warmth of the ... Pediatrics Read More Showing Slide 1 of 7 The post Incrementum Conference 2026: Revolutionizing Emergency Medicine in Spain appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 🗝️ Key Points 💨 Master the 3 Types of BreathsControl, Assist, and Spontaneous — know the difference before tackling ventilator modes.📦 Breath Delivery: Volume vs. PressureVolume-Targeted = fixed volume → monitor pressure📈 Pressure-Targeted = fixed pressure → monitor volume🫁 Lung Compliance = Pressure-Volume RelationshipVolume mode: ↑ pressure = ↓ compliance (stiff lungs)Pressure mode: ↓ tidal volume = ↓ compliance Click here for Direct Download of the Podcast. 📝 Introduction For 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 Breaths To 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 DeliveryThe 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 DeliveryThe 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 PressureIn 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 Line Before tackling advanced ventilator modes, master these foundational concepts:The three breath typesThe two delivery methodsThe role of lung complianceOnce 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, MD Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Nicole Ebalo, DO Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Showing Slide 1 of 2 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes appeared first on REBEL EM - Emergency Medicine Blog.

🧭 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 Podcast00:07 First Encounter with Intraosseous Lines01:09 Advantages of Intraosseous Lines02:42 Intraosseous Lines in Pediatric Patients03:34 Optimal Locations for Intraosseous Lines06:17 Limitations and Considerations07:34 Conclusion and Final Thoughts 📝 Introduction Welcome 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. 🧠 Background The 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 IOProximal tibia may be easier to landmark than proximal humerusOther sites include distal tibia, distal femur and sternum but are uncommonly employed in EDs 🚰 Flow Rates Proximal Humerus IO~300cc over 5 minutesFaster than tibiaMay be harder to access in some trauma or positioning scenarios Tibial IO~200cc over 5 minutesSlower flow compared to humerusEasier to access, especially during CPR or transport Sternal IOUp to 500cc over 5 minutesHighest flow rateBest for rapid volume resuscitationRisk 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 contraindicatedBlood work drawn from an IO are generally not accurate, so once the patient has been resuscitated with the IO, intravenous blood draws are recommendedDislodgement 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 Line Intraosseous 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, MPH All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Cast Episode 28: Refractory Ventricular Fibrillation Background: Welcome back to the September 2016 REBEL Cast. We ... Cardiovascular Read More REBEL Cast Episode 27: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia Background: In the ACLS guidelines stable Ventricular Tachycardia (VT) can ... Cardiovascular Read More REBEL Cast Episode 26: Advice to the Graduating Resident – Victoria Brazil So this is the third installation of Advice to the Graduating ... Read More REBEL Cast Episode 24: Advice to the Graduating Resident – Amal Mattu So this is the second installation of Advice to Graduating ... Read More REBEL Cast Episode 23: Is ST-Segment Elevation in Lead aVR Getting Too Much Respect? with Amal Mattu Lead aVR is a commonly ignored lead and I have ... Cardiovascular Read More REBEL Cast Episode 22: Advice to the Graduating Resident – Anand Swaminathan We are getting closer to the end of the year ... Read More Showing Slide 1 of 7 The post REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine appeared first on REBEL EM - Emergency Medicine Blog.

🧭 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. 📝 Introduction On 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 Decompression00:17 Recognizing Tension Pneumothorax01:00 Common Scenarios for Pneumothorax01:34 Confirming Diagnosis with POCUS01:50 Issues with Needle Decompression03:21 Advantages of Finger Thoracostomy04:11 Key Takeaways and Conclusion 📚 References 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: 16244336Laan 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: 26724173Terboven 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, MPH All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Cast Episode 20: All Cardiology Episode Welcome to the December 2015 REBELCast, where Swami, Matt, and I ... Cardiovascular Read More REBEL Cast Episode 17: The All Thoracotomy Episode Welcome to the October 2015 REBELCast, where Swami, Matt, and I ... Resuscitation Read More REBEL Cast Episode 15: MET for Renal Colic & Use of Broselow Tape to Estimate Pediatric Weights Welcome to the August 2015 REBEL Cast, where Swami, Matt, and I ... Pediatrics Read More REBEL Cast Episode 14: Early Cardiac Catheterization in OHCA Survivors with Non-STEMI Background: We know that cardiac arrest is a devastating disease ... Cardiovascular Read More REBEL Cast Episode 12: Bootcamp Edition – Delayed Sequence Intubation Welcome back to a special edition, or should I say ... Resuscitation Read More REBEL Cast Episode 10: Corticosteroids in Allergic Reactions/Anaphylaxis & Age of PRBCs in Critically Ill Adults Welcome to the May 2015 REBELCast, where Swami, Matt, and I ... Allergy and Immunology Read More Showing Slide 1 of 7 The post REBEL Core Cast 139.0: Pneumothorax Decompression appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 🧠 Shock is a Clinical Diagnosis — Not Just a NumberPatients can be in compensated shock with normal BP. Look for signs like AMS, cool extremities, ↓ UOP, and ↑ HR/RR.🖐️ Start with the 4 L’sLucid (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 BedsideQuick vitals, focused history, and targeted exam can reveal the etiology faster than invasive tools. Click here for Direct Download of the Podcast. 📝 Introduction In 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 Concepts What is Shock? Supply vs. Demand mismatch:Inadequate perfusion relative to metabolic demandsLeading to tissue hypoxia and cell death DO2 = CO x (Hb x Sat + (0.003 x paO2))CO = Heart Rate x Stroke VolumeDeterminants 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 ShockIncreased HR, increased RR, AMS, decreased urine output, cool to touch, weak pulses, slow capillary refill Defining Blood Pressure 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 PressureSBP – 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 DBPPneumothoraxIncreased intrathoracic pressure ➡️ decrease IVC and SVC ➡️ decreased preload Cardiac TamponadeFluid in pericardial space ➡️ decrease filling ➡️ decreased preloadPulmonary 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 vitalsWhy 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 Line A 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, MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Micheal Bass DO Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC Frank J. Lodeserto MD Associate Professor and Internal Medicine Residency Program Director Adult & Pediatric Critical Care Medicine, Cape Fear Valley Medical Center, Fayetteville, NC Showing Slide 1 of 3 🔎 Your Deep-Dive Starts Here REBEL Core Cast 129.0 – Gastric Lavage Take Home Points Orogastric lavage may still play an important ... Toxicology Read More REBEL Core Cast 128.0 – Toxic Alcohols Take Home Points Toxic alcohols generally refer to methanol and ... Toxicology Read More REBEL Core Cast 127.0 – Penetrating Neck Injuries Take Home Points Anticipate anatomically challenging airways and consider early ... Trauma Read More A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection Can AI spot occlusive MI on a single 12-lead ECG ... Cardiovascular Read More REBEL Core Cast 126.0 – Peds Hem Onc Emergencies Take Home Points Early administration of antibiotics (within 60 min) ... Hematology and Oncology Read More REBEL Core Cast 125.0 – Hyperkalemia Take Home Points Always obtain an EKG in patients with ... Endocrine, Metabolic, Fluid, and Electrolytes Read More Showing Slide 1 of 7 The post REBEL Core Cast 138.0: A Simple Bedside Approach to Shock appeared first on REBEL EM - Emergency Medicine Blog.

🧭 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. 📝 Introduction Sinus 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 Tachycardia Airway/Hypoxia: Ensure the airway is patent and assess for hypoxemia. Breathing: Evaluate for respiratory distress or pulmonary pathology.Circulation: Consider shock states, including hypovolemia, hemorrhage, or distributive shock. Drugs: Review medications and substances that may cause tachycardia, including stimulants and withdrawal states.Erythrocytes (Anemia): Assess for low hemoglobin levels that may impair oxygen delivery. Fever: Recognize that fever increases metabolic demand, leading to tachycardia.Glucose: Identify hypoglycemia or hyperglycemia as potential contributors.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 Line Sinus 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, MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Thirumala “Keerthi” Kammaripalle, MD Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC Showing Slide 1 of 2 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points Short + shallow: Neuromuscular, bronchospasm, or compliance problem → act fast ⚠️Normal/large tidal volume: Compensation for metabolic/systemic causeUse all tools: 👁 Eyes: Chest rise, ✋ Hands: Palpate,👂 Ears: Listen, 🧠 Brain: Synthesize Click here for Direct Download of the Podcast. 📝 Introduction In 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 Concepts First 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 Buckets Neuromuscular DiseaseMyasthenia gravis crisis, Guillain-Barré, myopathies, frailty.Weak inspiratory effort leads to low tidal volumes.Needs urgent positive pressure support (BiPAP, or intubation).Severe BronchospasmAsthma, 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.Worsening Lung Compliance“Stiff lungs” harder to ventilate.Compliance (C) = Δ Volume / Δ PressureSo if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is lowCauses 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 Causes Metabolic Acidosis (e.g., DKA)Compensatory hyperventilation (Kussmaul breathing)Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosisRespiratory AlkalosisCauses: Pain, anxiety, fever, early sepsis, CNS issuesCentral drive increases respiratory rateAgain, ABG or VBG helps confirmDead Space VentilationPulmonary 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 ventilationKey concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.  🛌 Practical Bedside Approach Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issueThink: Impending respiratory failure, act quickly.Normal to large tidal volumes? Systemic causesThink: Compensation (acidosis, pain, anxiety, PE).Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize). 🚨 Clinical Bottom Line A 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, MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Micheal Bass DO Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC Showing Slide 1 of 2 🔎 Your Deep-Dive Starts Here REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy Take Home Points Management of severe beta-blocker and calcium-channel blocker ... Toxicology Read More REBEL Core Cast 123.0 – Posterior Epistaxis Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. ... Head, Eye, Ear, Nose, and Throat Read More ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal Background: In May of 2018, Andexanet alfa gained accelerated approval ... Hematology and Oncology Read More REBEL Core Cast 122.0 – Neutropenic Fever Take Home Points: There are many causes of neutropenia, chemotherapy ... Infectious Disease Read More REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA? Background: The holy grail of outcomes in OHCA is survival ... Resuscitation Read More REBEL Core Cast 121.0 – Acute Sinusitis Take Home Points Acute rhinosinusitis is a clinical diagnosis The ... Head, Eye, Ear, Nose, and Throat Read More Showing Slide 1 of 7 The post REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient appeared first on REBEL EM - Emergency Medicine Blog.

🧭 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 needed️ V/Q mismatch🩸 Shunt (refractory to oxygen therapy) Click here for Direct Download of the Podcast. 📝 Introduction In 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 Concepts Hypoxemia 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 Hypoxia Hypoxemic Hypoxia: Blood oxygen is low, so tissues get less oxygen. (e.g., severe pneumonia)Anemic Hypoxia: Low hemoglobin levels mean less oxygen-carrying capacity, even if oxygen levels are normal. (e.g., hemorrhage, hemolysis)Ischemic Hypoxia: Blood flow to tissues is blocked or reduced. (e.g., MI, stroke, severe shock)Histotoxic Hypoxia: Oxygen delivery is normal, but tissues can’t use it. (e.g., carbon monoxide or cyanide poisoning) Five Major Causes of Hypoxemia 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.High AltitudeLower barometric pressure = less available oxygen, despite 21% FiO₂.Rarely relevant inside hospitals, but important to know.Diffusion DefectImpaired 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.V/Q Mismatch (Dead Space Disease)Problem with perfusion relative to ventilationCommon 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 tachypneicShunt (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 Line Mastering 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 MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Meet The Team 🔎 Your Deep-Dive Starts Here REBEL EM Book Club – MicroSkills Podcast Direct Download: Link Release Date: April 16th, 2024 Show ... Read More REBEL Cast – EMTALA + Reproductive Health Rights REBEL Cast – EMTALA + Reproductive Health Click here for ... Ethical and Legal Read More REBEL Cast Ep125: 1st 48 Hours of PE Management – How Good Is Unfractionated Heparin? Background: The mainstay of treatment for symptomatic pulmonary embolism  (PE) ... Cardiovascular Read More REBEL Cast Ep124: Nitrates in Right Sided MIs? Background: Nitrates can help improve symptoms and ischemia in the ... Cardiovascular Read More REBEL Core Cast 118.0 – IM vs PO NSAIDs REBEL Core Cast 118.0 – IM vs PO NSAIDs Click ... Read More REBEL Core Cast 117.0 – Infections of Pregnancy Take Home Points Infections are a leading cause of maternal ... Obstetrics and Gynecology Read More Showing Slide 1 of 7 The post REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) appeared first on REBEL EM - Emergency Medicine Blog.

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 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. Given the lack of a toxidrome, there should be a low threshold to obtain a screening acetaminophen concentration in the undifferentiated poisoned patient. 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. 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). 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. 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 Hendrickson RG, McKeown NJ. Chapter 33. Acetaminophen. In: Nelson LS, et al., editors. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019. 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 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 King’s College Criteria for Acetaminophen Toxicity. Available at: https://www.mdcalc.com/calc/532/kings-college-criteria-acetaminophen-toxicity#next-steps 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 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 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 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 The post REBEL Core Cast 134.0 – Acetaminophen Toxicity appeared first on REBEL EM - Emergency Medicine Blog.

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 Unhoused Click 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: Street Medicine Institute National Healthcare for the Homeless Council EMRA Fellowship Guide: Opportunities for Emergency Physicians, 3rd ed. The post Street Medicine: Compassionate Care for the Unhoused appeared first on REBEL EM - Emergency Medicine Blog.

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 Arthrotomy Click 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 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 131.0 – Traumatic Arthrotomy appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Early diagnosis: erythema and warmth of the skin surrounding the umbilicus isn’t normal. Get labs, start abx and get the patient admitted Consult peds surgery on all of these patients as progression to nec fast, while uncommon, is devastating 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 – Omphalitis Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 130.0 – Omphalitis appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points 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. 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. Secure the airway prior to placing the lavage tube to minimize aspiration risk. REBEL Core Cast 129.0 – Gastric Lavage Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 129.0 – Gastric Lavage appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Toxic alcohols generally refer to methanol and ethylene glycol as these substances pose significant metabolic derangement and end-organ damage. 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. 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. 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. Management includes fomepizole, hemodialysis, and vitamin supplementation.   REBEL Core Cast 128.0 – Toxic Alcohols Click 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) Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 128.0 – Toxic Alcohols appeared first on REBEL EM - Emergency Medicine Blog.

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 Injuries Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 127.0 – Penetrating Neck Injuries appeared first on REBEL EM - Emergency Medicine Blog.

Background: Cath lab activation based on ST-elevation myocardial infarction (STEMI) criteria is founded on aging data and requires evolution. In the “Occlusive Myocardial Infarction (OMI) Manifesto,” emergency physicians Dr. Steve Smith, Dr. Pendell Meyers, and Dr. Scott Weingart introduced a new paradigm —OMI vs. non-occlusive myocardial infarction (NOMI). The OMI/NOMI paradigm focuses on the presence of coronary occlusion, while STEMI/NSTEMI categorizes myocardial infarctions based on electrocardiogram (ECG) findings. Patients with OMI exhibit higher mortality and worse left ventricular function compared to those with NOMI.1, 2, 3 Detecting OMI is more difficult and necessitates scrutiny of the ECG, which is challenging in a busy emergency department where ED clinicians are interrupted more than ten times per hour.4, 5 Some OMI ECG signs include ST elevation in only one lead, subtle ST elevation with minimal reciprocal changes, isolated ST depressions, and hyperacute T waves. To meet this challenge, Dr. Steve Smith, Dr. Pendell Meyers (Dr. Smith’s ECG Blog), and their team developed The Queen of Hearts, a machine-learning AI model that has the potential to aid in the early detection of subtle OMI ECG changes. Accurately identifying OMI changes in ECG that STEMI criteria might otherwise miss would allow for more timely intervention, potentially salvaging more myocardium. An AI model that is highly sensitive in detecting OMI while maintaining a high degree of specificity would be an ideal tool to support emergency physicians’ clinical decision-making. The performance of this tool is unknown. Click here for Direct Download of the Podcast. Paper: Herman R, Meyers HP, Smith SW, et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Digit Health. 2023;5(2):123-133. Published 2023 Nov 28. PMID: 38505483 Clinical question: “Can an AI model detect an OMI lesion using a single 12-lead ECG?” What They Did: Investigators performed a retrospective derivation study followed by validation on an internal data set from the same Acute Coronary Syndrome (ACS) database. Cases eligible for inclusion were randomly assigned to a model development training set (derivation set) and testing set (validation set).   The training set included ECG feature extraction and classification Feature extraction used 60,000 parameters The classification component combined all extracted features and used an additional 150,000 parameters. The validation data set was used for hyperparameter tuning and threshold selection.  Investigators then tested the AI model on two data sets An internal European data set (internal validation set) A separate US data set (external validation set) from the DOMI ARIGATO database. They compared the AI model with the existing criteria for detecting OMI on 12-lead ECGs and analyzed the AI model in various subgroups. Population: Derivation Set: Random selection of ACS patients from the Cardiovascular Centre Aalst in Belgium and ACS patients from an international image database patient. EU Internal Test Set: Random Selection of ACS patients from the Cardiovascular Centre Aalst in Belgium and ACS patients from an international image database patient. US External Test Set: Patients from the DOMI ARIGATO database. Exclusion: ECGs >24 h before CAG and post-CAG ECGs with poor signal quality  ECGs with missing Expert Annotation, undigitizable ECGs, Baseline ECGs (additionally excluded from the US External Database) Intervention: AI-powered ECG model implemented on ECGs from the internal EU and external US datasets. Comparator: Blinded physician annotations of the standard ‘STEMI criteria’ on ECG Blinded subjective ECG expert annotations of OMI Angiographic clinical outcome data Outcomes: Primary Outcome: AI model’s ability to identify patients with angiographically confirmed OMI using only the 12-lead ECG. Secondary Outcomes: OMI AI model performance across demographic and ECG subgroups A comparison of the AI model performance against the existing STEMI criteria for detecting acute coronary occlusion from 12-lead ECGs A sensitivity analysis of AI model performance using various angiographic and laboratory cut-offs of OMI An evaluation of misclassified cases Results: The derivation set used in the AI model development included 18,616 ECGs from 10,543 patients with clinically validated outcomes. The overall test set included 3254 ECGs from 2222 patients   The internal EU testing cohort 2016 ECGs from 1630 patients  The US testing cohort 1238 ECGs from 633 patients  The prevalence of OMI differed between the internal EU and the external US test sets, 16% compared with 36.2%, respectively ( < 0.001). The patients in the US test set were younger, had more ECGs recorded before catheterization, and were more likely to present with a STEMI-positive ECG. AI Model Performance: Achieved an Area Under the ROC Curve (AUC) of 0.938 [95% CI: 0.924–0.951]. Accuracy: 90.9% [95% CI: 89.7–92.0]. Sensitivity: 80.6% [95% CI: 76.8–84.0]. Specificity: 93.7% [95% CI: 92.6–94.8]. STEMI Criteria Performance: STEMI criteria accuracy: 83.6% [95% CI: 82.1–85.1]. Sensitivity: 32.5% [95% CI: 28.4–36.6]. Specificity: 97.7% [95% CI: 97.0–98.3]. ECG Experts Performance: Accuracy of ECG experts was 90.8% [95% CI: 89.5–91.9]. Sensitivity: 73.0% [95% CI: 68.7–77.0]. Specificity: 95.7% [95% CI: 94.7–96.6]. OMI AI Model vs. STEMI Criteria: The OMI AI model performs significantly better than the STEMI criteria in sensitivity, Negative Predictive Value (NPV), Matthews correlation coefficient (MCC), and AUC. However, it has lower specificity and Positive Predictive Value (PPV) compared to the STEMI criteria. OMI AI Model vs. ECG Experts: The OMI AI model has higher sensitivity and NPV than ECG experts. It shows equal performance in AUC and is adjudicated as equal overall to ECG experts. Specificity and PPV are lower than ECG experts, and MCC is neutral. ECG Experts vs. STEMI Criteria: ECG experts have higher sensitivity, NPV, MCC, and AUC than STEMI criteria. They perform the same in specificity and PPV compared to STEMI criteria, leading to significantly better adjudication. Strengths: Rigorous Methodological Approach: The study follows a comprehensive methodological approach, encompassing stages of development, validation, and comparison. Large and Diverse Dataset: The model was trained and tested on a substantial dataset of 18,616 ECGs from 10,543 patients with ACS across multiple international cohorts. This diversity enhances the model’s generalizability and robustness. Expert Interpretation and Validation: All cases in the derivation set included expert ECG interpretations alongside clinically validated angiographic outcome data, ensuring high accuracy in the model’s training process. High Agreement Among Experts: Two authors, serving as ECG experts, annotated all tracings for the presence of OMI while being blinded to all clinical data. They achieved a 94% agreement (kappa = 0.849), demonstrating the reliability of the expert annotations. Independent Review: Blinded independent clinical reviewers adjudicated all angiographic data in the EU internal testing set, adding an extra layer of objectivity and reliability to the validation process. Comprehensive Performance Comparison: The study compares the AI model’s performance with existing STEMI criteria and expert ECG interpretations. This sets a quantifiable humanistic standard, highlighting the AI model’s enhanced performance. Limitations: Applicability Limited to ACS Patients: The AI model was developed using patients and ECGs exclusively from ACS databases, restricting its applicability to only those with ACS. Disease-Oriented Outcomes: The outcomes in this study are disease-oriented. While facilitating the diagnosis of OMI may lead to improved patient-oriented outcomes, this was not directly studied. Limited Generalizability to Asymptomatic Patients: The study is not generalizable to a broader population of asymptomatic patients and was not designed to quantify other relevant clinical endpoints such as mortality, in-hospital complications, or major adverse cardiovascular events (MACE). Lack of Prospective Validation: The validation set was analyzed retrospectively, lacking prospective validation to confirm the model’s effectiveness in real-world clinical settings. Randomization Process Not Mentioned: The randomization process used to allocate cases to the derivation or validation set is not mentioned, which may impact the robustness of the findings. Comparison Limited to 12-Lead ECG: The AI model was compared to the 12-lead ECG alone. Some patients undergo emergency angiography without clear STEMI criteria based on the full clinical picture. Therefore, the interpretation of the overall gain is limited without a pragmatic comparison to real-world clinical practices and patient-oriented outcomes. Limited Generalizability to Younger Population and Women: Approximately 10% of ECGs were from patients ≤45 years of age, and three-quarters of the cases were from males, limiting the generalizability to younger populations and women. Inappropriate Use of P-Values: The inclusion of p-values in Tables 1 and 2 is puzzling, as this is not a randomized controlled trial (RCT). Demographic differences between validation sets are expected and desired for external validity. Variability in Care Standards: Significant differences in clinical presentation and management between patients in Europe and the USA (e.g., the USA had younger patients and more ECGs before catheterization) could affect the model’s performance across different healthcare systems. Subjective Outcome Verification: The detection of OMI relied on visual verification of TIMI flow on angiograms, which may be subjective. Conflict of Interest: The lead author disclosed a conflict of interest as the co-founder and Chief Medical Officer of Powerful Medical. Other authors have disclosed employee or shareholder status in Powerful Medical. Discussion: Inside the Numbers: The data for this AI model is impressive, showcasing a remarkable capability in early and accurate detection of OMI on ECGs, demonstrating a sensitivity of 80.6% (76.8–84.0) and specificity of 93.7% (92.6–94.8). The AI model not only surpassed the standard STEMI ECG criteria [sensitivity 32.5% (28.4–36.6) and specificity 97.7% (97.0–98.3)] but also matched the performance of Dr. Steve Smith and Dr. Pendell Meyers, two well known ECG experts [sensitivity 73.0% (68.7–77.0) and specificity 95.7% (94.7–96.6)]. Additionally, when considering the existing evidence, the AI model would likely outperform ED physicians’ and cardiologists’ ability to detect ischemia on ECG, who achieved sensitivities of approximately 65% and specificities ranging from 65–79% in multiple studies.7, 8, 9 This high accuracy demonstrates AI’s potential to improve diagnostic processes and patient outcomes in emergency settings. The AI model’s PPV in this study was 0.780 (0.742–0.816), and the NPV was 0.946 (0.935–0.957) for the primary outcome. PPV and NPV are heavily influenced by disease prevalence, and a high prevalence increases the PPV, indicating that a positive test result is more likely to be a true positive. The 16% and 36.2% prevalence of OMI in the internal and external validation sets are likely much higher than expected from a random group of patients assessed for ACS in the ED on any given day. Consequently, the PPV is likely lower in a less risky population with a lower prevalence for ACS.   The AI model’s AUC for detecting OMI was 0.938 (0.924–0.951), with an optimal threshold of 0.1106. The optimal threshold refers to the chosen point that maximizes the AI model’s accuracy. The point is a probability that ranges from 0–1. However, investigators must choose the value (optimal threshold) at which the model determines whether the ECG is positive or negative. Therefore, the optimal threshold converts a continuous variable (probability) into a binary decision, such as distinguishing between the presence or absence of OMI on ECG. If the threshold is set too low, it might result in high sensitivity but low specificity, leading to many false positives. The ROC curve is a graphical plot that illustrates the diagnostic ability of a binary classifier as its discrimination threshold is varied. In this instance, a ROC curve with an AUC of 0.938 is outstanding and highlights the potential of the AI model to optimize clinical decision-making processes. Critical Biases and Considerations: The primary flaw in this paper is selection bias. All patients included in the derivation and validation sets were selected from ACS databases. As mentioned, the prevalence of OMI in the internal and external validation sets is very high. Physicians should exercise caution when applying this data more broadly (i.e., all patients with an ECG in the ED).  The AI model detected OMI in 979 cases total, 267 of which also met the STEMI criteria on ECG. Therefore, 27% of the OMIs detected by the AI model might have been more obvious and less noteworthy to an emergency physician aiming to improve their diagnostic capabilities. However, the remaining 73% of AI-detected OMIs are particularly interesting because they require meticulous ECG scrutiny for accurate diagnosis. While not all these AI-detected OMI cases met the primary outcome criteria, technology can fill a void in identifying patients who may benefit from emergent intervention despite the lack of STEMI-specific criteria on ECG. “Time is myocardium,” and the primary goal in ACS treatment is to detect OMI on ECG as early as possible to prevent myocardial necrosis. Utilization of STEMI criteria missed 330 OMI patients —false negatives. Among these, 133 had a median revascularization time of 9.3 hours but were correctly identified by the AI model on the first ECG. Early detection can potentially improve patient outcomes, especially in cases with real-world median angiography time of 9 hours. While this data is compelling, it highlights the need for prospective evaluation of the AI model compared to the performance of the average emergency physician to fully assess its clinical effectiveness. The Future and Transformative Potential of AI: This AI model’s development and validation process mirrors that of a clinical decision instrument, beginning with retrospective derivation followed by internal and external validation. Before widespread implementation, prospective validation in various clinical settings with diverse populations is necessary. Additionally, utilization studies should confirm that the AI model achieves its intended goals, such as earlier detection of OMI and improved patient-oriented outcomes. While the idea of AI taking over the world might be an exaggeration, its transformative impact cannot be overstated. The continuous advancement and integration of AI technologies can lead to more efficient, accurate, and personalized solutions. Moreover, AI’s continuous refinement through machine learning suggests its performance will only improve over time. As the AI model is exposed to more data and varied cases, it can refine its algorithms, enhance its accuracy, and adapt to new patterns, making it an invaluable tool in the medical field. And, unlike human counterparts, AI will not fatigue and will maintain high accuracy levels, even after the 12th hour on duty and dozens of ECG interpretations. The possibilities for AI applications in healthcare are virtually limitless.  Author’s conclusion: “AI model outperformed gold-standard STEMI criteria in the diagnosis of OMI, but further prospective clinical studies are needed to define the role of the OMI AI model in guiding ACS triage and the timely referral of patients benefiting from immediate revascularization.” Clinical Bottom Line: The Queen of Hearts AI model demonstrates impressive accuracy, surpassing STEMI criteria and matching expert interpretation for detecting OMI on ECG. However, the high prevalence of OMI in the study’s datasets may overestimate AI’s ability to detect OMI in a general ED population with a lower disease prevalence. Ultimately, the model requires prospective validation in diverse clinical settings before widespread adoption— but this could be a winning hand. References: Wang TY, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. 2009;157(4):716-723. PMID: 19332201 Pride YB, Tung P, Mohanavelu S, et al. Angiographic and clinical outcomes among patients with acute coronary syndromes presenting with isolated anterior ST-segment depression: a TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) substudy. JACC Cardiovasc Interv. PMID: 20723851 Khan AR, Golwala H, Tripathi A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2017;38(41):3082-3089. PMID: 29020244 Ratwani RM, Fong A, Puthumana JS, Hettinger AZ. Emergency Physician Use of Cognitive Strategies to Manage Interruptions. Ann Emerg Med. 2017;70(5):683-687. PMID: 28601266 Chisholm CD, Dornfeld AM, Nelson DR, Cordell WH. Work interrupted: a comparison of workplace interruptions in emergency departments and primary care offices. Ann Emerg Med. 2001;38(2):146-151. PMID: 11468609 Herman R, Meyers HP, Smith SW, et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Digit Health. 2023;5(2):123-133. Published 2023 Nov 28. PMID: 38505483 Veronese G, Germini F, Ingrassia S, et al. Emergency physician accuracy in interpreting electrocardiograms with potential ST-segment elevation myocardial infarction: Is it enough?. Acute Card Care. 2016;18(1):7-10. PMID: 27759433 McCabe JM, Armstrong EJ, Ku I, et al. Physician accuracy in interpreting potential ST-segment elevation myocardial infarction electrocardiograms. J Am Heart Assoc. 2013;2(5):e000268. Published 2013 Oct 4. PMID: 24096575 Paez Perez Y, Rimm S, Bove J, et al. Does the Electrocardiogram Machine Interpretation Affect the Ability to Accurately Diagnose ST-Elevation Myocardial Infarction by Emergency Physicians?. Crit Pathw Cardiol. 2023;22(1):8-12. PMID: 36812338 Guest Post By: Marco Propersi, DO FAAEM Vice-Chair, Emergency Medicine Assistant Emergency Medicine Residency Program Director Vassar Brothers Hospital, Poughkeepsie, New York Twitter/X: @marco_propersi Joseph Bove, DO FAAEM Associate Director Emergency Medicine Co-Director of the EM Residency Clerkship St. Joseph’s University Medical Center Email: [email protected] Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami) The post A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection appeared first on REBEL EM - Emergency Medicine Blog.

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 Emergencies Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 126.0 – Peds Hem Onc Emergencies appeared first on REBEL EM - Emergency Medicine Blog.

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 – Hyperkalemia Click 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 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 125.0 – Hyperkalemia appeared first on REBEL EM - Emergency Medicine Blog.

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 Therapy Click 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 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. 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. HIET therapy requires simultaneous dextrose and potassium infusions as insulin will induce hypoglycemia and shift potassium intracellularly. If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered. References 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 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 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 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy appeared first on REBEL EM - Emergency Medicine Blog.

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 Epistaxis Click 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 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 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 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 Viducich RA et al. Posterior epistaxis: clinical features and acute complications. Acad Emerg Med 1995; 25(5): 592-6. PMID: 7741333 Corrales CE, Goode RL. Should patients with posterior nasal packing require ICU admission. Laryngoscope 2013; 123: 2928-9. PMID: 24114977 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 123.0 – Posterior Epistaxis appeared first on REBEL EM - Emergency Medicine Blog.

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 Reversal Click 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: 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 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) The post ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal appeared first on REBEL EM - Emergency Medicine Blog.

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 Fever Click 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: 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. 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 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. Ellis M. Febrile Neutropenia. Annals of New York Academy of Sciences. 2008 Sep;1138:329-50. doi: 10.1196/annals.1414.035. 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. 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. Gorschlüter M, Mey U, Strehl J, et al. Neutropenic enterocolitis in adults: systematic analysis of evidence quality. Eur J Haematol 2005; 75:1. 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 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 Klastersky J. Management of fever in neutropenic patients with different risks of complications. Clin Infect Dis. 2004;39(Suppl. 1):S32–S37 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. 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 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 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) The post REBEL Core Cast 122.0 – Neutropenic Fever appeared first on REBEL EM - Emergency Medicine Blog.

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: 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) The post REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA? appeared first on REBEL EM - Emergency Medicine Blog.

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 Sinusitis Click 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 Anon JB et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004; 130(Suppl 1): 1-45. PMID: 14726904 Lemiengre MB et al. Antibiotics for Clinically Diagnosed Acute Rhinosinusitis in Adults. Cochrane Database Syst Rev 2012. PMID: 23076918 Berg O et al. Occurence of asymptomatic sinusitis in common cold and other acute ENT-infections. Rhinology 1986; 24(3): 223-5. PMID: 3775189 Gwaltney JM. Acute community-aquired sinusitis. Clin Infect Dis 1996; 23(6): 1209-23. PMID: 8953061 Ahovuo-Saloranta A et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev 2008. PMID: 18425861 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) The post REBEL Core Cast 121.0 – Acute Sinusitis appeared first on REBEL EM - Emergency Medicine Blog.

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) The post REBEL EM Book Club – MicroSkills appeared first on REBEL EM - Emergency Medicine Blog.