REBEL EM – Emergency Medicine Blog

By Salim R. Rezaie, MD

Rational Evidence-Based Evaluation of Literature... more

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How many episodes does REBEL EM – Emergency Medicine Blog have?

The podcast currently has 18 episodes available.

REBEL EM – Emergency Medicine Blog episodes:

July 21, 2025REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia
🧭 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

🔎 Your Deep-Dive Starts Here

REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia

Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ...

Cardiovascular

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REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient

In this episode, we focus on the bedside evaluation of ...

Thoracic and Respiratory

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REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia)

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

Resuscitation

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REBEL Core Cast 1.0 – The Intro

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

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The Approach To The Most Common Cardiac Dysrhythmia: 8 Causes of Sinus Tachycardia

Have you ever heard an entire lecture on sinus tachycardia? ...

Cardiovascular

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18min
July 07, 2025REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient
🧭 REBEL Rundown

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

📝 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 Disease
Myasthenia gravis crisis, Guillain-Barré, myopathies, frailty.
Weak inspiratory effort leads to low tidal volumes.
Needs urgent positive pressure support (BiPAP, or intubation).
Severe Bronchospasm
Asthma, COPD, anaphylaxis.
Shallow, forced expirations signal airway obstruction.
Silent Chest = airway emergency.
Treat with bronchodilators, steroids, and positive pressure ventilation.
Avoid immediate intubation if reversible; trial NIPPV first.
Worsening Lung Compliance
“Stiff lungs” harder to ventilate.
Compliance (C) = Δ Volume / Δ Pressure
So if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is low
Causes include:
Chest Wall: Rigidity, burn eschar.
Pleural Space: Effusion, pneumothorax (check for asymmetric chest rise).
Lung Parenchyma: Pneumonia, contusion, atelectasis.
Below the Lung: Abdominal distension, ascites.
Clinical pearl: Work outside-in (chest wall, pleura, lung, abdomen).
Normal to High Tidal Volumes with Tachypnea: Systemic Causes
Metabolic Acidosis (e.g., DKA)
Compensatory hyperventilation (Kussmaul breathing)
Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosis
Respiratory Alkalosis
Causes: Pain, anxiety, fever, early sepsis, CNS issues
Central drive increases respiratory rate
Again, ABG or VBG helps confirm
Dead Space Ventilation
Pulmonary embolism (PE) is the classic cause.
Other causes include:
Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but under perfused areas.
Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation
Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.
🛌 Practical Bedside Approach
Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issue
Think: Impending respiratory failure, act quickly.
Normal to large tidal volumes? Systemic causes
Think: Compensation (acidosis, pain, anxiety, PE).
Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize).
🚨 Clinical Bottom 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

🔎 Your Deep-Dive Starts Here

MDCalc Wars: Stop Before the CT! — Are You Using PERC or Wells Correctly

Diagnosing PE in the emergency department is tricky. The symptoms—chest ...

Thoracic and Respiratory

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Casting Doubt: The SUSPECT Trial — Bandaging Vs. Casting for Suspected Occult Scaphoid Fracture

Managing patients with suspected occult scaphoid fractures and normal X-rays ...

Orthopedics

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Combination Inhalers in Asthma: Time to Switch?

🧭 REBEL Rundown 📌 Key Points 💨 Most asthma patients ...

Thoracic and Respiratory

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The ADAPT-Sepsis Trial: Biomarker-Guided Antibiotic Duration for Hospitalized Patients with Suspected Sepsis

Antibiotic stewardship entails delivering the most appropriate antimicrobial therapy for ...

Infectious Disease

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REBEL Core Cast 134.0 – Acetaminophen Toxicity

Acetaminophen (APAP) overdose remains one of the most common causes ...

Toxicology

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MDCalc Wars: NEXUS Criteria Vs Canadian C-Spine Rules

Over 1 million blunt trauma patients visit US emergency departments ...

Trauma

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The post REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient appeared first on REBEL EM - Emergency Medicine Blog.
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16min
June 16, 2025REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia)
🧭 REBEL Rundown

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

📝 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 Altitude
Lower barometric pressure = less available oxygen, despite 21% FiO₂.
Rarely relevant inside hospitals, but important to know.
Diffusion Defect
Impaired oxygen transfer across alveoli, often due to chronic lung disease.
Examples: interstitial lung disease, idiopathic pulmonary fibrosis.
Patients are usually known to have underlying disease.
V/Q Mismatch (Dead Space Disease)
Problem with perfusion relative to ventilation
Common examples:
Pulmonary embolism (classic dead space).
Other causes include:
Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.
Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.
Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but unperfused areas.
Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation.
Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.
Key point: Patients often oxygenate “ok” at rest but are tachypneic
Shunt (Most Common and Most Concerning)
“Crap in the alveoli” blocks oxygen diffusion:
Pneumonia (pus)
Pulmonary edema (water)
Atelectasis (collapse)
Pulmonary hemorrhage (blood)
Blood moves from right to left without being oxygenated.
Refractory hypoxemia despite oxygen therapy = shunt physiology.
Key Move: High FiO₂ (non-rebreather mask) → if still hypoxemic, they need positive pressure (NIV or intubation).
🛌 Practical Bedside Approach
Give as much FiO₂ as possible (non-rebreather mask).
Watch SpO₂ response:
If it improves → V/Q mismatch or dead space more likely.
If it doesn’t improve → think shunt physiology.
If refractory hypoxemia persists → Start positive pressure ventilation (HFNC, CPAP, BiPAP, or intubation depending on the situation).
🚨 Clinical Bottom 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

Is 7 Days Enough? Rethinking Antibiotic Duration in Sepsis — The BALANCE Trial

Current IDSA guidelines for sepsis recommend individualized durations of antibiotic ...

Infectious Disease

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TNK vs tPA — The ORIGINAL Trial

The American Heart Association and the European Stroke Organization have ...

Neurology

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How Accurate are Blood Gas Electrolyte Measurements?

Bottom Line Up Top: Blood gas electrolytes closely correlate with ...

Endocrine, Metabolic, Fluid, and Electrolytes

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Size Matters: The Impact of Cuff Size on Blood Pressure

Background: Accurate blood pressure (BP) measurement is essential in the ...

Procedures and Skills

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Street Medicine: Compassionate Care for the Unhoused

Introduction: In this episode of Rebel Cast, host Marco Propersi, ...

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Is the D-Dimer Useful in High-Probabilty Pulmonary Embolism?

Bottom Line Up Top: A negative D-Dimer likely excludes significant ...

Cardiovascular

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The post REBEL Core Cast 135.0: A Simple Approach to Hypoxemia (vs. Hypoxia) appeared first on REBEL EM - Emergency Medicine Blog.
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20min
June 02, 2025REBEL Core Cast 134.0 – Acetaminophen Toxicity
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
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19min
April 02, 2025Street Medicine: Compassionate Care for the Unhoused
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.
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56min
November 13, 2024REBEL Core Cast 131.0 – Traumatic Arthrotomy
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.
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7min
October 30, 2024REBEL Core Cast 130.0 – Omphalitis
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.
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6min
October 16, 2024REBEL Core Cast 129.0 – Gastric Lavage
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.
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7min
October 02, 2024REBEL Core Cast 128.0 – Toxic Alcohols
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.
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17min
September 18, 2024REBEL Core Cast 127.0 – Penetrating Neck Injuries
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.
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10min

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The podcast currently has 18 episodes available.