EM Pulse Podcast™

Caring for patients with severe traumatic brain injury (TBI)—especially pediatric patients—is high-stakes and high-stress. In severe TBI, primary brain injury occurs at the moment of impact; our primary goal in the emergency department is preventing secondary brain injury caused by hypoxia, hypoperfusion, elevated intracranial pressure (ICP), seizures, hyperthermia, and dysglycemia. In this episode, ED Clinical Pharmacist Haley Burhans returns to walk us through key medications for the acute management of severe TBI. We’ll cover airway management, rapid sequence intubation (RSI) drug choices, hyperosmolar therapy, seizure prophylaxis, TXA, and post-resuscitation care. 1. Airway & Rapid Sequence Intubation (RSI) Optimizing oxygenation and ventilation is critical, as hypoxemia directly contributes to secondary brain injury. Selecting hemodynamically neutral agents is essential to maintain cerebral perfusion pressure (CPP). Induction Agents Etomidate (0.3 mg/kg, max 40 mg): Hemodynamically neutral, making it a reliable choice for TBI patients with unstable or uncertain blood pressures. Ketamine (1–2 mg/kg): Excellent option for borderline low or hypotensive patients. Historical concerns regarding ketamine-induced ICP spikes have been largely disproven; bolus doses <5 mg/kg do not cause sustained ICP elevations and offer valuable analgesia. Paralytics Succinylcholine (1.5 mg/kg TBW, max 200 mg): Preferred if an immediate post-intubation neurological exam is required by neurosurgery, given its short duration (~10–15 min). Rocuronium (1.0–1.2 mg/kg): Higher dosing ensures rapid onset. Preferred when securing the airway smoothly and keeping the patient still for immediate CT scanning is the priority. Note: Paralyzes the patient for 45–60 minutes, so obtain a baseline neuro exam first or have a plan for reversal if an early exam is needed. Pre-Medications (Lidocaine vs. Fentanyl) Lidocaine (1.5 mg/kg): Theoretically blunts airway-reflex-induced ICP spikes during intubation, but takes 2–5 minutes to reach peak effect and introduces cardiac risks in undifferentiated trauma patients. Generally omitted when rapid airway placement is required. Fentanyl (1–2 mcg/kg): Preferred pre-medication for hypertensive or tachycardic patients to blunt sympathetic surges and prevent ICP spikes during laryngoscopy. 2. Post-Intubation Sedation & Hemodynamic Support Hypotensive / Unstable: Push-dose Ketamine (1–2 mg/kg) provides deep sedation while preserving blood pressure. Hypertensive / Stable: Propofol infusion (Adults: ~40 mcg/kg/min; Pediatrics: ~60 mcg/kg/min due to faster metabolism) helps suppress ICP and optimize CPP. Pressors: If vasopressors are required to maintain target SBP (>100–110 mmHg depending on age), titrate carefully to clear hemodynamic goals. Avoid reflexively starting high-dose pressors if transient hypotension was primarily driven by hypoxia or cardiac arrest before airway placement. 3. Seizure Prophylaxis Post-traumatic seizures increase metabolic demand and elevate ICP. First-Line Agent: Levetiracetam (Keppra) is non-inferior to Phenytoin for preventing early post-traumatic seizures (within 7 days) and carries a significantly lower risk of cardiac side effects and agitation at standard loading doses. Dosing: Loading Dose: 20–25 mg/kg IV load (common adult loading dose is 20 mg/kg or a standard 1,000–2,000 mg IV dose). Maintenance: 25 mg/kg IV BID in pediatrics; 1,000 mg IV BID in adults (adjusted for renal function). 4. Hyperosmolar Therapy for Cerebral Edema When signs of impending herniation or acute ICP elevation are present: Hypertonic Saline (3% NaCl): Pediatrics: First-line agent at 2–5 mL/kg IV. Avoids the diuretic/hypovolemic risks associated with mannitol in volume-dependent pediatric patients. Adults: Strongly preferred over mannitol due to less rebound ICP elevation and easier administration (mannitol requires inline filters and can crystallize). Mannitol (0.5–1 g/kg): Alternative option in adults, but can cause osmotic diuresis, hypotension, and rebound ICP increases. Combining/Redosing: Avoid giving both hypertonic saline and mannitol simultaneously as initial therapy—if the patient deteriorates 30 minutes later, therapeutic options are exhausted. Hypertonic saline is easier to redose safely after monitoring serum sodium levels (peak effect around 1 hour). 5. Role of Tranexamic Acid (TXA) Isolated TBI in Adults: The CRASH-3 trial showed potential 30-day mortality benefits for mild-to-moderate TBI within 3 hours of injury, but limited clear benefit in isolated severe TBI. If a severe TBI is an isolated injury, routine TXA push is not strongly advocated if it delays primary line access for other resuscitation meds. Polytrauma / Pediatrics: If TBI is part of multi-trauma or severe pediatric trauma within 3 hours of injury, TXA is appropriate as part of overall trauma resuscitation protocols. 6. Critical ED Targets & Common Pitfalls Temperature Management: Target strict normothermia (36.0°C–38.0°C). Fevers (>38°C) double metabolic demand and worsen secondary brain injury. Consider bundling IV acetaminophen into post-RSI orders. Glucose Control: Avoid extreme hyperglycemia; treat severe elevations (>200 mg/dL or noted high levels on VBG) early in the ED. Communication & Lines: Hyperosmolar agents are incompatible with many continuous infusions. Clearly communicate upper and lower blood pressure limits with nursing to avoid over-titrating antihypertensives or sedatives. What are your go-to meds for severe TBI? What do you avoid? Share your experience with us on social media @empulsepodcast or at ucdavisem.com Hosts: Dr. Julia Magaña, Professor of Pediatric Emergency Medicine at UC Davis Dr. Sarah Medeiros, Professor of Emergency Medicine at UC Davis Guests: Haley Burhans, PharmD, Emergency Medicine Clinical Pharmacist at UC Davis Resources: ACEP Critical Care Medicine: Key Aspects in the Management of TBI in the ED to Minimize Secondary Injury by Miyant’e Newton, MD, March 12, 2024 Brain Trauma Foundation Guidelines for the Management of Severe TBI, 4th Edition Brain Trauma Foundation Guidelines for the Management of Pediatric Severe TBI, 3rd Edition **** Thank you to the UC Davis Department of Emergency Medicine for supporting this podcast and to Orlando Magaña at OM Productions for audio production services.

Ultrasound-guided nerve blocks are no longer just a niche skill for fellowship-trained ultrasound specialists—they are a core component of modern multimodal pain management in the ED. Endorsed by ACEP, nerve blocks can offer rapid, targeted pain relief without relying solely on systemic opioids, making everything from rest to imaging and procedural workups significantly more comfortable for patients. Today, Dr. Carlos Mikell, UC Davis Emergency Ultrasound Faculty and nerve block expert, joins us to share why every emergency physician should adopt nerve blocks as part of their practice. We’ll break down the top ED blocks, explore innovative indications like genicular nerve blocks for knee pain, and discuss essential safety protocols and how to get started – or become more comfortable – with blocks in your ED. Why Nerve Blocks Belongs in the ED Targeted Relief: Delivers effective, localized pain management as part of a multi-modal pain control approach, sparing patients some of the systemic side effects of opioids. Facilitates ED Workup: Relieves movement-related pain, making imaging, patient transport, and local procedures far easier and more comfortable for the patient. ACEP Endorsement: ACEP’s policy statement formalizes ultrasound-guided nerve blocks as an essential skill for all emergency physicians—not just ultrasound fellowship graduates. Analgesia, Not Complete Anesthesia: The goal in the ED is regional analgesia (taking pain down to a manageable, functional level safely) rather than dense, surgical anesthesia. The Most Common ED Nerve Blocks According to data from the National Ultrasound Guided Nerve Block Registry: Fascia Iliaca Plane / Femoral Nerve Block (~36%): Indications: Hip fractures, mid-shaft/distal femur fractures, hip dislocations, and severe thigh trauma. Safety Profile: Highly safe; target plane is centimeters away from the main neurovascular bundle in a easily compressible site. Erector Spinae Plane (ESP) Block: Indications: Back pain, renal colic, shingles, and rib fractures. Forearm Blocks (Median, Ulnar, Radial): Indications: Distal forearm fractures, complex lacerations, and hand procedures. Serratus Anterior Plane (SAP) Block (~7%): Indications: Rib fractures, pre/post-chest tube insertion pain, and chest wall abscesses. Tip: Hydro-dissect with normal saline first to identify the fascial plane before injecting local anesthetic, and consider adding dexamethasone to extend duration. Innovative Block Spotlight: Genicular Nerve Block Target: Three of the primary sensory branches of the sciatic/femoral nerves supplying the anterior knee. Indications: Acute knee trauma/fractures, acute-on-chronic knee pain, and severe osteoarthritic flare-ups. Safety & Execution: Low-volume block (~10 mL total). Pearl: Omit the inferior-lateral genicular injection to avoid unintentional peroneal nerve block and foot drop. Streamlining Nerve Blocks in Your Department To move nerve blocks from a rare procedure to a routine clinical tool: ED Infrastructure: Build standardized EMR order sets, procedure note templates, and dedicated nerve block supply carts/kits. Departmental Support: Designate a point person to coordinate credentialing, interdisciplinary pathways (e.g., trauma, orthopedics), and physician/nurse/tech education. Hands-on Training: Utilize cadaver labs, simulation, and scanning shifts to build faculty and resident confidence. Non-Negotiable Safety Guidelines & LAST Prevention Nerve blocks are generally low-risk, but vigilance is critical to avoid complications like Local Anesthetic Systemic Toxicity (LAST) or direct nerve injury: Patient Selection: Avoid in uncommunicative patients (who cannot report paresthesias or tinnitus), areas at high risk for compartment syndrome, or pre-existing severe nerve deficits. Monitoring: Keep patients on cardiac telemetry for 30–60 minutes post-block for central or high-volume blocks (>10 mL or above the elbow/knee). Dosing Buffer: Calculate maximum weight-based local anesthetic doses every time; stay within 60–70% of the maximum dose to maintain a safety buffer. Intralipid Availability: Ensure 20% Intralipid is immediately accessible in the ED pharmacy or brought directly to the bedside. Injection Technique: Never point the needle directly at a nerve. Inject into the fascial plane, stop immediately if you encounter resistance, and perform frequent aspirations every 3–5 mL. What is your favorite ultrasound-guided nerve block? What barriers do you encounter to doing blocks in the ED? We’d love to hear form you! Connect with us on social media @empulsepodcast or connect with us on ucdavisem.com Hosts: Dr. Julia Magaña, Professor of Pediatric Emergency Medicine at UC Davis Dr. Sarah Medeiros, Professor of Pediatric Emergency Medicine at UC Davis Guest: Dr. Carlos Mikell, Assistant Professor of Emergency Medicine and Ultrasound Faculty at UC Davis Resources: ACEP Policy Satement: Ultrasound Guidelines: Emergency, Point-of-care, and Clinical Ultrasound Guidelines in Medicine, June 2016 ACEP Now: How To Build an Ultrasound-Guided Nerve Block Program By Arun Nagdev, MD; Kaitlen Howell, MD; Akash Desai, MD; David Martin, MD; and Daniel Mantuani, MD, MPH | on January 6, 2023  ACEP Sonoguide: Nerve Blocks NURVE Block Registry Brown J, Milgrim F, Driver L, et al. Efficacy and Safety of Adjunct Medications in ED Ultrasound-Guided Nerve Blocks: A National Ultrasound-Guided NeRVE (NURVE) Block Registry Study. Acad Emerg Med. 2025 Dec;32(12):1299-1308. doi: 10.1111/acem.70128. Epub 2025 Aug 27. PMID: 40873157. Goldsmith A, Driver L, Duggan NM, et al. Complication Rates After Ultrasonography-Guided Nerve Blocks Performed in the Emergency Department. JAMA Netw Open. 2024 Nov 4;7(11):e2444742. doi: 10.1001/jamanetworkopen.2024.44742. Erratum in: JAMA Netw Open. 2024 Dec 2;7(12):e2455847. doi: 10.1001/jamanetworkopen.2024.55847. PMID: 39535792; PMCID: PMC11561692. *** Thank you to the UC Davis Department of Emergency Medicine for supporting this podcast and to Orlando Magaña at OM Productions for audio production services. Disclaimer: The opinions expressed on this podcast are those of the hosts or guests and do not necessarily reflect the views of UC Davis Department of Emergency Medicine, UC Davis Health, or their parent organizations.

The Outbreak With over 17,000 cases reported across the U.S., a massive Cyclospora outbreak has taken center stage in public health news, marking it as the third-largest foodborne outbreak in modern American history (behind the 1994 Schwan’s ice cream salmonella outbreak and the 1985 Illinois milk outbreak). Infection causes gastrointestinal symptoms, including diarrhea, bloating, nausea and sometimes vomiting.  So, what’s actually driving this surge? Is it safe to eat salad? Pediatric infectious disease expert Dr. Dean Blumberg joins us to break down the science behind the “explosive” symptoms, separate real outbreak epicenters from everyday travel cases, and when to test and treat. Transmission & Geography  Mechanism: Cyclospora is a parasite. It is often transmitted via produce contaminated with sewage or irrigation water.  Not Person-to-Person: Requires ~1 week in the environment to mature and become infectious.  Regional Risk: The epicenter for this outbreak is in the Midwest, related to processed lettuce distribution networks. Outside affected regions, cases remain at expected baseline levels (primarily tied to international travel). Fresh produce consumption remains safe.  Pathophysiology & Presentation  Cellular Damage: Cyclospora infects and kills small intestine epithelial cells, impairing fluid absorption and causing unabsorbed carbohydrates to ferment into gas.  Symptoms: Large-volume, gas-driven “explosive” diarrhea, abdominal bloating, and cramping. Fever is rare; vomiting is variable.  Duration: Unlike viral gastroenteritis (1–3 days), untreated Cyclospora can linger for weeks and frequently waxes and wanes. Diagnostic Strategy Routine “O&P x3” tests are obsolete—use multiplex PCR panels (e.g., GI BioFire).  When to Test: Symptoms lasting >5–7 days, high-risk patients (infants <12 months, older adults, immunocompromised), fever, bloody stool, or symptoms seriously impacting daily life. (Negative panels can help rule out infectious causes and prompt work up for other etiologies, such as IBD)  When to Skip: Patients with 1–2 days of mild symptoms or the “worried well.” Treatment  First-Line Agent: Trimethoprim-sulfamethoxazole (TMP-SMX / Bactrim).  Indication: Treat anyone who tests positive and remains actively symptomatic to speed recovery and prevent relapses.  Reporting: Confirmed cases are automatically reported to public health by the lab.  Primary Complication: Severe dehydration and electrolyte derangements (the main drivers of hospitalization). Have you seen many Cyclospora cases? Or an influx of concerned patients with mild GI symptoms?  Share your experience with us on social media @empulsepodcast or at ucdavisem.com Hosts: Dr. Julia Magaña, Professor of Pediatric Emergency Medicine at UC Davis Dr. Sarah Medeiros, Professor of Emergency Medicine at UC Davis Guests: Dr. Dean Blumberg, Chief of Pediatric Infectious Diseases at UC Davis Resources: CDC: Cyclosporiasis AAP News: CDC offers guidance on cyclosporiasis outbreaks for clinicians, public    July 14, 2026 Melissa Jenco, Senior News Editor *** Thank you to the UC Davis Department of Emergency Medicine for supporting this podcast and to Orlando Magaña at OM Productions for audio production services.

Cannabinoid Hyperemesis Syndrome (CHS) continues to be a major clinical challenge in the emergency department. Patients present with severe abdominal pain, intractable vomiting, and significant fluid and electrolyte derangements. CHS often affects people who have been using cannabis routinely for months to years – it can be difficult for patients to understand that their symptoms are related to cannabis.  Today, emergency pharmacist Haley Burhans joins us to discuss first-line treatments, fluid management, discharge strategies, and how to navigate these tough bedside conversations. First-Line Therapies: Haldol vs. Droperidol Haloperidol (Haldol): Supported by the HAVOC trial (haloperidol vs. placebo), which showed a reduction in symptoms and ED length of stay. Droperidol: Highly effective alternative with similar dopaminergic mechanism of action. May carry a lower risk of extrapyramidal symptoms compared to haloperidol.  Capsaicin Cream: addresses the TRPV1 pathway thought to drive CHS. Patients often dislike it as it causes a burning sensation on the skin and can be inadvertently spread to eyes or face. Can be an option if symptoms persist after trying the above meds and hot showers aren’t feasible.  Backup Options & Anti-Emetics Alternative Dopaminergic Agents: Metoclopramide or prochlorperazine can be used. Standard Anti-Emetics (e.g., Ondansetron): Serotonergic anti-emetics generally fail to address the underlying CHS pathway. However, a single dose of ondansetron given alongside a butyrophenone (haloperidol/droperidol) is reasonable if you suspect co-existing etiologies. QTc Prolongation Warning: Chronic vomiting leads to electrolyte depletion. Combining anti-emetics and haloperidol or droperidol increases the risk of QTc prolongation. Baseline EKG: Not strictly required for every low-risk patient, but strongly recommended for patients with multiple risk factors (e.g., co-ingestion/use of methadone, history of heart failure, or severe baseline bradycardia). Fluid Resuscitation & Electrolyte Management CHS patients can vomit to the point of severe dehydration and profound electrolyte/acid-base derangements. Fluid Selection: Normal Saline (NS): A solid choice for initial volume resuscitation when sodium and chloride are severely depleted. Lactated Ringer’s (LR): Ideal as a follow-up or maintenance fluid because it contains a small amount potassium. Potassium Repletion: Oral repletion may not be tolerated in the acute setting. Consider IV potassium repletion in the ED, followed by oral home supplementation once nausea is controlled. Magnesium: While acute vomiting primarily drives potassium loss, consider IV magnesium if Mg is low or there is concern for QTc prolongation. Discharge Planning: What to Send Home Low-Dose Olanzapine ODT: Send the patient home with 2.5 mg Olanzapine ODT (orally disintegrating tablets). Why it works: It dissolves instantly on the tongue, bypassing the stomach, and provides extended dopaminergic coverage over the multi-day washout period.  Pharmacokinetics Pearl: Infrequent user THC half-life: ~1.3 hours (cleared in 5–6 hours). Chronic user THC half-life: THC accumulates in adipose tissue. In heavy users, therapeutic levels can persist for up to 2 weeks, driving prolonged receptor dysregulation even after cessation. Navigating the Bedside Conversation Explaining to a chronic user that their daily cannabis—the very thing they use to relieve nausea—is causing their illness requires empathy and validation. Explain the Neurological Link: Cannabis acts on receptors throughout the entire body, including the brain’s nausea center and the nervous system of the gut. Chronic, heavy saturation can paradoxically overload these pathways. Validate Their Experience: Acknowledge how counterintuitive it feels: “I know it’s hard to believe that something you’ve used for years to feel better is causing this, but long-term daily use can change how your body processes it.” Set Realistic Expectations: Reiterate that symptoms will not resolve overnight. Even after stopping, it takes time for the pathways to recalibrate. What do you find most helpful for treating CHS? How do you have these difficult conversaions with your patients? Share your experience with us on social media @empulsepodcast or at ucdavisem.com Hosts: Dr. Julia Magaña, Professor of Pediatric Emergency Medicine at UC Davis Dr. Sarah Medeiros, Professor of Emergency Medicine at UC Davis Guests: Haley Burhans, PharmD, Emergency Medicine Clinical Pharmacist at UC Davis Resources: Borgundvaag B, Bellolio F, Miles I, et al. Guidelines for Reasonable and Appropriate Care in the Emergency Department (GRACE-4): Alcohol use disorder and cannabinoid hyperemesis syndrome management in the emergency department. Acad Emerg Med. 2024 May;31(5):425-455. doi: 10.1111/acem.14911. PMID: 38747203. Rech MA, Shalaby M, Gage KA, Gottlieb M. Managing Cannabinoid Hyperemesis Syndrome. Ann Emerg Med. 2026 Jun;87(6):717-722. doi: 10.1016/j.annemergmed.2025.12.024. Epub 2026 Feb 3. PMID: 41632059. *** Thank you to the UC Davis Department of Emergency Medicine for supporting this podcast and to Orlando Magaña at OM Productions for audio production services.

A landmark international trial published in the New England Journal of Medicine evaluated whether fluid type impacts patient outcomes.