Core EM - Emergency Medicine Podcast

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Core EM - Emergency Medicine Podcast

Core EM is dedicated to bringing Emergency Providers all things core content Emergency Medicine. In the true spirit of Emergency Medicine our content is available to anyone, anywhere, anytime.

  1. 2 DÉC.

    Acetaminophen Toxicity

    We sit down with one of our toxicologists to discuss acetaminophen toxicity. Hosts: Marlis Gnirke, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acetaminophen_Toxicity.mp3 Download Leave a Comment Tags: Toxicology Show Notes Table of Contents 0:35 – Hidden acetaminophen toxicity in OTC products 3:24 – Pharmacokinetics and toxicokinetics  6:06 – Clinical Course 9:22 – The antidote – NAC 11:02 – The Rumack-Matthew Nomogram  17:36 – Treatment protocols 22:34 – Monitoring and Lab Work 23:23 – Considerations when treating pediatric patients 23:57 – IV APAP overdose, fomepizole  25:42 – Take Home Points Acetaminophen vs. Tylenol: The importance of recognizing that acetaminophen is found in many products beyond Tylenol. Common medications containing acetaminophen, such as Excedrin, Fioricet, Percocet, Dayquil/Nyquil, and others. The risk of unintentional overdose due to combination products. Prevalence of Acetaminophen Toxicity: Widespread availability and under-recognition contribute to its prevalence. The potential for unintentional overdose when taking multiple medications containing acetaminophen. Pharmacokinetics and Metabolism: Normal metabolism pathways of acetaminophen and the role of glutathione. Formation of the toxic metabolite NAPQI during overdose situations. Saturation of safe metabolic pathways leading to hepatotoxicity. Pathophysiology of Liver Injury: How excessive NAPQI leads to hepatocyte death, especially in zone III of the liver. The difference between therapeutic dosing and overdose metabolism. Clinical Stages of Acetaminophen Toxicity: Stage 1: Asymptomatic or nonspecific symptoms (first 24 hours). Stage 2: Onset of hepatic injury (24-72 hours), elevated AST/ALT. Stage 3: Maximum hepatotoxicity (72-96 hours), signs of liver failure. Stage 4: Recovery phase, complete hepatic regeneration if survived. Antidote – N-Acetylcysteine (NAC): Mechanisms of NAC in replenishing glutathione and detoxifying NAPQI. The importance of early administration, ideally within 8 hours post-ingestion. NAC’s role even in late presenters and in fulminant hepatic failure. The Rumack-Matthew Nomogram: How to use the nomogram for acute overdoses to determine the need for NAC. Limitations in chronic overdoses and late presentations. Emphasis on obtaining accurate time of ingestion and acetaminophen levels. Treatment Protocols: Standard 21-hour IV NAC protocol and dosing specifics. Managing anaphylactoid reactions associated with IV NAC. Criteria for extending NAC therapy beyond 21 hours.

  2. 1 NOV.

    Sexually Transmitted Infections 2.0

    We review Sexually Transmitted Infections and pertinent updates in diagnosis and management. Hosts: Avir Mitra, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Sexually_Transmitted_Infections_2_0.mp3 Download Leave a Comment Tags: gynecology, Infectious Diseases, Urology Show Notes Table of Contents (1:49) Chlamydia  (3:31) Gonorrhea (4:50) PID (6:14) Syphilis (8:08) Neurosyphilis  (9:13) Tertiary Syphilis (10:06) Trichomoniasis  (11:13) Herpes (12:49) HIV (14:10) PEP (15:13) Mycoplasma Genitalium  (18:00) Take Home Points Chlamydia: * Prevalence: Most common STI. High percentage of asymptomatic cases (40% to 96%). * Presentation: Urethritis, cervicitis, pelvic inflammatory disease (PID), prostatitis, proctitis, pharyngitis, arthritis. Importance of considering extra-genital sites (oral and rectal infections). * Testing: Gold Standard: Nucleic Acid Amplification Test (NAAT) via PCR. * Sampling Sites: Endocervical or urethral swabs preferred over urine samples due to higher sensitivity. Triple-site testing (genital, rectal, pharyngeal) recommended for comprehensive detection. * Treatment Updates: Previous Regimen: Azithromycin 1 g orally in a single dose. Current First-Line Treatment: Doxycycline 100 mg orally twice daily for 7 days. * Alternatives: Azithromycin remains an option for patients unlikely to adhere to a 7-day regimen or for pregnant patients. Note: PID treatment differs and will be discussed separately. Gonorrhea: * Presentation: Similar to chlamydia; can be asymptomatic. Symptoms include urethritis, cervicitis, PID, prostatitis, proctitis, pharyngitis. * Testing: Gold Standard: NAAT. * Sampling Sites: Endocervical swabs are more sensitive than urine samples. Triple-site testing is crucial to avoid missing infections.

  3. 1 OCT.

    Migraines

    We discuss migraines with one of the authorities in the field. Hosts: Benjamin Friedman, MD of Montefiore Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Migraines.mp3 Download Leave a Comment Tags: Neurology Show Notes Initial Approach to Diagnosing Migraines: * Differentiating between primary headaches (migraine, tension-type, cluster) and secondary causes (e.g., subarachnoid hemorrhage). * The importance of patient history and reevaluation after initial treatment. * Recognizing the unique presentation of cluster headaches and their management implications. Effective Acute Migraine Treatments: * First-line treatments including anti-dopaminergic medications like metoclopramide (Reglan) and prochlorperazine (Compazine), and parenteral NSAIDs like ketorolac (Toradol). * The limited role of triptans in the ED due to side effects and less efficacy compared to anti-dopaminergics. * The use of nerve blocks (greater occipital nerve block and sphenopalatine ganglion block) as effective treatments without systemic side effects. Treatments to Avoid or Use with Caution: * Diphenhydramine (Benadryl): Studies show it does not prevent akathisia from anti-dopaminergics nor improve migraine outcomes. * IV Fluids: Routine use is not supported unless the patient shows signs of dehydration. * Magnesium: Conflicting evidence with some studies showing no benefit or even harm. Managing Refractory Migraines: * Second-line treatments including additional doses of metoclopramide combined with NSAIDs or dihydroergotamine (DHE). * Considering opioids as a last resort when other treatments fail. * The potential use of newer medications like lasmiditan and CGRP antagonists. Preventing Recurrence of Migraines: * Administering a single dose of dexamethasone (4 mg IV) to reduce the risk of headache recurrence after discharge. * Prescribing NSAIDs or triptans upon discharge for outpatient management. * Recognizing and addressing chronic migraine, and initiating preventive therapies like propranolol when appropriate. Key Takeaways * Differentiate Primary from Secondary Headaches and Reassess After Treatment: * Use patient history and reevaluation post-treatment to distinguish migraines from more serious conditions, reducing unnecessary imaging and procedures. * First-Line Treatments Are Effective: * Anti-dopaminergic medications and NSAIDs are the mainstay of acute migraine treatment in the ED. * Reserve opioids for cases unresponsive to multiple lines of treatment. * Avoid Unnecessary Interventions: * Diphenhydramine and routine IV fluids do not have proven benefits and can be excluded to streamline care. * Utilize Nerve Blocks for Refractory Cases: * Greater occipital nerve blocks and sphenopalatine ganglion blocks are ...

  4. 2 SEPT.

    Immune Checkpoint Inhibitors

    We discuss a new class of medications, Immune Checkpoint Inhibitors, and their side effects. Hosts: Avir Mitra, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Immune_Checkpoint_Inhibitors.mp3 Download Leave a Comment Tags: Oncology Show Notes Overview of Immune Checkpoint Inhibitors (ICIs) ICIs are a relatively new class of oncologic drugs that have revolutionized cancer treatment. Unlike chemotherapy, ICIs help the immune system develop memory against cancer cells and adapt as the cancer mutates. Since their release in 2011, ICIs have expanded to 83 indications for 17 different cancers, with approximately 230,000 patients using them. Mechanism of Action Cancer cells can evade the immune system by binding to T cell receptors that downregulate the immune response. ICIs work by blocking these receptors or ligands, preventing the downregulation and allowing T cells to proliferate and attack cancer cells. Common ICIs Risks and Toxicities of ICIs ICIs can lead to autoimmune attacks on healthy cells due to immune system upregulation. Immune-related adverse effects (irAEs) include colitis, pneumonitis, dermatitis, hepatitis, and endocrine issues (e.g., hypothyroid, hypocortisolemia, hypophysitis). These toxicities can present as infections, making diagnosis challenging in the emergency room. Management of ICI Toxicities in the ER Diagnosis: Look for signs that mimic infections (e.g., cough and fever in pneumonitis). Diagnostic Imaging in pneumonitis: If CXR is normal but suspicion is high, consider CT scans to differentiate conditions like pneumonitis from other issues such as malignancy-associated pleural effusion or acute pulmonary embolism. Treatment: The primary treatment for irAEs is steroids (e.g., prednisone 1 mg/kg). Start steroids early and hold the ICI to manage symptoms effectively and increase the likelihood of resuming ICI therapy later. Consider using antibiotics in combination with steroids if there is uncertainty about whether symptoms are due to infection or ICI toxicity. Coordinate care with the patient’s oncologist if possible Disposition Decisions Patient disposition (admit vs. discharge) should depend on clinical presentation and severity. Coordination with oncology is crucial; they are often comfortable with starting steroids even if there is a potential infection. Patients can be discharged if symptoms are mild, but sicker patients with more complex presentations may require admission. Take-Home Points ICIs are a new class of cancer drugs that effectively target cancer cells but come with unique immune-related toxicities. Diagnosing irAEs can be challenging due to symptom overlap with infections. The cornerstone of treatment is early administration of steroids and temp...

  5. 1 AOÛT

    Ataxia In Children

    We discuss a case of ataxia in children and how to approach the evaluation of these pts. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Ataxia_in_Children.mp3 Download Leave a Comment Tags: Neurology, Pediatrics Show Notes Introduction * The episode focuses on ataxia in children, which can range from self-limiting to life-threatening conditions. * Pediatric emergency medicine specialist shares insights on the topic. The Case * An 18-month-old boy presented with ataxia, unable to keep his head up, sit, or stand, and began vomiting. * Previously healthy except for recurrent otitis media and viral-induced wheezing. * The decision to take the child to the emergency department (ED) was based on acute symptoms. Differential Diagnosis * Common causes include acute cerebellar ataxia, drug ingestion, Guillain-Barre syndrome, and basilar migraine. * Less common causes include cerebellitis, encephalitis, brain tumors, and labyrinthitis. Importance of History and Physical Examination * A detailed history and physical exam are essential in diagnosing ataxia. * Key factors include time course, recent infections, signs of increased intracranial pressure, and toxic exposures. * Look for signs such as bradycardia, hypertension, vomiting, and overall appearance. Diagnostic Workup * Initial tests include point-of-care glucose and neuroimaging for concerns about trauma or increased intracranial pressure. * MRI is preferred for posterior fossa abnormalities, but non-contrast head CT is commonly used due to accessibility. * Lumbar puncture may be needed if meningismus is present. Treatment Approach * Treatment depends on the underlying cause: * Acute cerebellar ataxia is self-limiting and typically resolves with time. * Antibiotics are required for meningitis or encephalitis. * Steroids may be useful for cerebellitis and acute disseminated encephalomyelitis (ADEM). * Specialist consultations are necessary for severe diagnoses like intracranial masses. Outcome of the Case Study * The child had a normal fast T2 MRI and improved during the ED stay. * Diagnosed with a combination of cerebellar ataxia and labyrinthitis. * Received myringotomy tubes and experienced no further neurologic changes or otitis media episodes. Take-Home Points * Diverse Etiologies:  Ataxia in children can have various causes that range from self-limiting to life-threatening * Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures. * Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may ...

  6. 1 JUIL.

    Hypernatremia

    We discuss the approach to diagnosing and managing hypernatremia in the emergency department. Hosts: Abigail Olinde, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hypernatremia.mp3 Download Leave a Comment Tags: Electorlye Show Notes Episode Overview: * Introduction to Hypernatremia * Definition and basic concepts * Clinical presentation and risk factors * Diagnosis and management strategies * Special considerations and potential complications Definition and Pathophysiology: * Hypernatremia is defined as a serum sodium level over 145 mEq/L. * It can be acute or chronic, with chronic cases being more common. * Symptoms range from nausea and vomiting to altered mental status and coma. Causes of Hypernatremia based on urine studies: * Urine Osmolality > 700 mosmol/kg * Causes: * Extrarenal Water Losses: Dehydration due to sweating, fever, or respiratory losses * Unreplaced GI Losses: Vomiting, diarrhea * Unreplaced Insensible Losses: Burns, extensive skin diseases * Renal Water Losses with Intact AVP Response: * Diuretic phase of acute kidney injury * Recovery phase of acute tubular necrosis * Postobstructive diuresis * Urine Osmolality 300-600 mosmol/kg * Causes: * Osmotic Diuresis: High glucose (diabetes mellitus), mannitol, high urea * Partial AVP Deficiency: Incomplete central diabetes insipidus * Partial AVP Resistance: Nephrogenic diabetes insipidus * Urine Osmolality 100 mEq/L * Causes: * Sodium Overload: Ingestion of salt tablets, hypertonic saline administration * Salt Poisoning: Deliberate or accidental ingestion of large amounts of salt * Mixed or Variable Urine Sodium * Causes: * Diuretic Use: Loop diuretics, thiazides * Adrenal Insufficiency: Mineralocorticoid deficiency * Osmotic Diuresis with Renal Water Losses: High glucose, mannitol Risk Factors: * Patients with impaired thirst response or those unable to access water (e.g., altered or ventilated patients) are at higher risk. * Important to consider underlying conditions affecting thirst mechanisms. Diagnosis: * Initial assessment includes history, physical examination, and laboratory tests.

  7. 3 JUIN

    Episode 197: Acute Agitation

    We discuss an approach to the acutely agitated patient and review medications commonly used. Hosts: Jonathan Kobles, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Agitation.mp3 Download Leave a Comment Tags: Agitation, psychiatry, Toxicology Show Notes Background/Epidemiology •Definition and Scope: Agitation encompasses behaviors from restlessness to severe altered mental states. It’s a common emergency department presentation, often linked with acute medical or psychiatric emergencies. •Significance: Patients with agitation are at high risk for morbidity and mortality, necessitating prompt and effective management to prevent harm to themselves and healthcare providers. A Changing Paradigm in Describing Agitation •Terminology Shift: Move away from terms like ‘excited delirium’ due to their politicization and stigmatization. Focus on describing agitation by severity and underlying causes. Agitation as a Multifactorial Process •Complex Nature: Recognize agitation as a result of various factors, including medical, psychiatric, and environmental influences. Recognizing Agitation •Signs and Symptoms: Identify agitation early by monitoring for behaviors such as hostility, pacing, non-compliance, and verbal aggression. Initial Evaluation •Severity Assessment: Determine the severity of agitation and prioritize reversible causes and life-threatening conditions. •Diagnostic Steps: Perform vital signs check, blood glucose levels, ECG, and a targeted medical screening exam. Life Threats •Immediate Concerns: Identify and address immediate life threats such as hypoxia, hypoglycemia, trauma, and acute neurological emergencies. Forming a Differential Prior to Treatment •Prioritization: Severe agitation requires immediate treatment to facilitate further evaluation and reduce risk of harm. Physician/Staff Safety •Safety Measures: Ensure personal and team safety by maintaining a calm environment and preparing for potential violence. Multimodal Approach •Self-check In: Physicians should mentally prepare and approach the situation calmly to ensure effective management. •Verbal De-escalation: Use techniques focused on safety, therapeutic alliance, and patient autonomy to manage agitation non-pharmacologically. Medication Administration •Oral/Sublingual Medications: Consider oral medications for less severe cases to maintain patient autonomy and avoid invasive procedures. •IM or IV Medications: Use intramuscular or intravenous medications for rapid control in severe cases. Specific Medication Regimens •PO Regimens: •Medications: Antipsychotics like Zyprexa (olanzapine) 5-10 mg, benzodiazepines like Ativan (lorazepam) 1-2 mg. •Benefits: Empower patients with a sense of autonomy, avoid injection-related trauma.

  8. 1 MAI

    The Critically Ill Infant

    We discuss an approach to the critically ill infant. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/The_Critically_Ill_Infant.mp3 Download Leave a Comment Tags: Pediatrics Show Notes The Critically Ill Infant: THE MISFITS Trauma * ‘T’ in the mnemonic stands for trauma, which includes both accidental and intentional causes. * Considerations for Non-accidental Trauma: * Stresses the importance of considering non-accidental trauma, especially given that it may not always present with obvious external signs. * Anatomical Vulnerabilities: * Highlights specific anatomical considerations for infants who suffer from trauma: * Infants have proportionally larger heads, increasing their susceptibility to high cervical spine (c-spine) injuries. * Their liver and spleen are less protected, making abdominal injuries potentially more severe. Heart * 5 T’s of Cyanotic Congenital Heart Disease: Introduces a mnemonic to help remember key right-sided ductal-dependent lesions: * Truncus Arteriosus: Single vessel serving as both pulmonary and systemic outflow tract. * Transposition of the Great Arteries: The pulmonary artery and aorta are switched, leading to improper circulation. * Tricuspid Atresia: Absence of the tricuspid valve, leading to inadequate development of the right ventricle and pulmonary circulation issues. * Tetralogy of Fallot: Comprises four defects—ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta. * Total Anomalous Pulmonary Venous Connection (TAPVC): Pulmonary veins do not connect to the left atrium but rather to the right heart or veins, causing oxygen-rich blood to mix with oxygen-poor blood. * Other Significant Conditions: * Ebstein’s Anomaly: Malformation of the tricuspid valve affecting right-sided heart function. * Pulmonary Atresia/Stenosis: Incomplete formation or narrowing of the pulmonary valve obstructs blood flow to the lungs. * Left-sided Ductal-Dependent Lesions: * Conditions such as aortic arch abnormalities (coarctation or interrupted arch), critical aortic stenosis, and hypoplastic left heart syndrome are highlighted. These generally present with less obvious cyanosis and more pallor. * Diagnostic and Management Considerations: * Routine prenatal ultrasounds detect most cases, but conditions like coarctation of the aorta and TAPVC might not be apparent until after birth when the ductus arteriosus closes. * Emphasizes the importance of a thorough physical exam: checking for murmurs, assessing hepatosplenomegaly, feeling for femoral pulses, measuring pre- and post-ductal saturations,

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Core EM is dedicated to bringing Emergency Providers all things core content Emergency Medicine. In the true spirit of Emergency Medicine our content is available to anyone, anywhere, anytime.

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