ERcast: Clinical Perspectives Podcast Preview

Hippo ERcast September 2023

  • Sep 2023
  • 9 Chapters
  • 3 hr 1 min

September 2023 ERcast starts off with a conversation about the use of steroids in the ED - the conditions we know they work for, those they do not work for, and a few where they may be helpful.  Next, Cam Berg shares an ADP for phenobarbital in alcohol withdrawal.  Brit Long walks us through acute chest syndrome, and then Neda Frayha and DeLaney discuss a practical approach to the treatment of neuropathic pain.  Meenal Sharkey makes her ERcast debut with a review of sarcoidosis diagnosis and management.  Drew and Andy remind us of the importance of keeping central lines sterile as they review a new set of guidelines.  In Lit Matters, we discuss steroid therapy in septic shock, patients’ perspectives on immediate access to test results through online portals, and the safety of high-dose nitroglycerin in SCAPE.  Enjoy!

Faculty

  • Andy Little, DO

    Dr. Andy Little is an emergency medicine physician and educator. He earned his medical degree from the Ohio University Heritage College of Osteopathic Medicine and completed his emergency medicine residency at OhioHealth Doctors Hospital Emergency Medicine Residency, where he served as Chief Resident. He has received multiple national awards, including recognition from the American Osteopathic Association, American College of Osteopathic Emergency Physicians, and Emergency Medicine Residents' Association.

  • Cameron Berg, MD

    Based in Minneapolis, MN, Dr. Berg focuses on simplifying complex patient care processes, such as chest pain, syncope, and heart failure treatment. Since 2020, he has also been navigating his own recovery from a TBI after a bicycle accident. When he isn't in the clinic, Cameron is usually busy keeping his three young children alive and happy.

  • Drew Kalnow, DO

    Dr. Drew Kalnow is an emergency medicine physician and educator based in Columbus, Ohio. He completed his emergency medicine training at OhioHealth Doctors Hospital Emergency Medicine Residency. Dr. Kalnow is passionate about advancing emergency medicine through high-quality education, with a particular focus on simulation, learning theory, and innovative teaching.

  • Matthew DeLaney, MD, FACEP, FAAEM

    Dr. Matthew DeLaney is an emergency medicine physician and educator based in Birmingham, Alabama. A native of Mobile, he earned his medical degree from the University of South Alabama and completed his emergency medicine residency at Maine Medical Center.Dr. DeLaney has experience in both community and academic emergency medicine and is known for his commitment to teaching and medical education. He lives in Birmingham with his wife, Erin, who is also a physician, and their two daughters.

  • Brit Long, MD

    Dr. Brit Long is a Professor of Emergency Medicine at the University of Virginia and an emergency medicine physician with experience in both a community ED and at a military academic center ED. He is the Clinical Editor-in-Chief of emDOCs.His professional interests include medical education, evidence-based medicine, and the FOAMed movement. Outside of work, he enjoys spending time with his wife and two daughters

  • Meenal Sharkey, MD
  • Neda Frayha, MD

Chapters

September Intro: 'Roid Rage'

Short-course oral corticosteroids are not benign; even a typical six-day outpatient burst is linked to sepsis, venous thromboembolism, and fracture. In emergency care, steroids clearly help in asthma, COPD, and croup, while evidence is weak, mixed, or absent for common cold, musculoskeletal pain, sinusitis, sciatica, migraine, and pharyngitis. Steroids in Emergency Care Short-course harm signal: A large cohort of 1.5 million adults found outpatient steroid bursts were common and associated with sepsis, venous thromboembolism, and fracture, a risk-benefit reset worth hearing in the episode. Best-supported indications: The clearest wins are asthma, COPD, and croup, where dexamethasone remains a high-yield ED steroid and a single dose can match longer bursts in obstructive disease. Route evidence gap: Oral dexamethasone performs as well as IM in moderate croup, and there is little evidence that routine IV or IM 'steroid shots' outperform PO for most common indications. Poor-use cases: There is no good evidence supporting steroids for acute musculoskeletal pain or the common cold, two settings where practice often runs ahead of data. Mixed-benefit syndromes: Sciatica may show modest functional improvement without meaningful pain relief, and adverse effects are common. We get into where that tradeoff may still matter on the show. Adjunctive symptom roles: For migraine, parenteral dexamethasone cuts recurrence by about 26%, and for pharyngitis steroids improve 24- to 48-hour symptom relief, but these are adjuncts rather than universal first-line moves.

Alcohol Withdrawal: How to Use Phenobarbital

Alcohol withdrawal syndrome is easy to undertreat and easy to make worse with inconsistent protocols. Diazepam remains a strong first-line benzodiazepine, and phenobarbital has a defined role in both early treatment and benzodiazepine-resistant withdrawal. Phenobarbital in Alcohol Withdrawal Institutional treatment consistency: A single alcohol withdrawal assessment and treatment pathway reduces shift-to-shift variability, a common reason these patients deteriorate despite repeated ED care. Diazepam as first choice: Diazepam is a practical benzodiazepine anchor because it is bioequivalent PO, IM, and IV, and can be dosed in 10 mg aliquots for escalating withdrawal. Dual role for phenobarbital: Phenobarbital is not just a rescue drug; it can be used up front for admitted withdrawal patients and again when benzodiazepines are failing. We get into the selection nuances in the episode. Headline phenobarbital doses: Severe or benzodiazepine-resistant withdrawal is paired with 260 mg IV phenobarbital, while lower-risk admitted patients may start with oral loading followed by a taper. Cumulative dose awareness: Phenobarbital has a cumulative dosing phenomenon that may not declare itself in the ED, making total dose tracking and pharmacist involvement especially important. High-risk combination cautions: Use extra caution in older adults, and avoid stacking phenobarbital with both benzodiazepines and opioids because synergistic sedation can become the real emergency.

Lit Matters 1: Single vs Dual Steroid Therapy in Septic Shock

Septic shock that remains vasopressor-refractory is the main setting where adjunctive corticosteroids enter the conversation. New comparative-effectiveness data suggest hydrocortisone plus fludrocortisone may outperform hydrocortisone alone, but the ED decision still hinges on timing, boarding, and how much protocol complexity you want to add up front. Dual Steroids in Septic Shock Vasopressor-refractory shock window: Adjunctive steroids matter after adequate perfusion attempts and ongoing vasopressor dependence, not as routine time-zero sepsis therapy; that ED timing distinction is worth hearing in the episode. Mineralocorticoid rationale: Fludrocortisone adds mineralocorticoid activity to hydrocortisone, a biologically plausible pairing for septic shock patients whose blood pressure remains stubborn despite vasopressors. Large emulation cohort: A Premier database target-trial emulation captured about 88,000 septic shock patients, giving this question a far larger real-world sample than the earlier dual-steroid trials. Headline mortality signal: Death or discharge to hospice was lower with combination therapy, roughly 47% versus 51% with hydrocortisone alone, a signal strong enough to keep the question alive. Secondary outcome direction: Vasopressor-free days and hospital length both moved in favor of dual therapy, with about a one-day improvement, though residual confounding still limits certainty. Practical ED adoption: For frontline emergency care, simplicity still competes with theory: a single inexpensive steroid such as dexamethasone may be the default, while prolonged boarding or escalating pressors may justify more.

High Risk, Low Prevalence: Acute Chest Syndrome

Acute chest syndrome is a high-mortality acute lung injury in sickle cell disease, and a normal initial chest x-ray does not exclude it. Early recognition hinges on new respiratory symptoms plus a new radiodensity somewhere on imaging, with lung ultrasound or CT stepping in when suspicion stays high. Recognizing Acute Chest Syndrome High mortality phenotype: Acute chest syndrome causes about 25% of deaths in sickle cell disease, and each episode carries roughly 9% mortality, making even subtle early presentations worth treating aggressively. Core diagnostic frame: Think ACS when fever or new respiratory symptoms in sickle cell disease are paired with a new segmental radiodensity on imaging, often alongside vaso-occlusive pain crisis. False-negative chest x-ray: A negative initial x-ray does not rule out ACS because consolidation commonly lags behind the clinical picture; we get into when ultrasound or CT should move up in the episode. Typical trigger patterns: Nearly half of cases have no identifiable trigger, but vaso-occlusive pain crisis is the leading adult precipitant while asthma is a common pediatric driver. Clues to severe disease: Multilobar involvement, neurologic symptoms, worsening hypoxemia, and rapid progression toward multiorgan injury should raise concern for the severe ACS phenotype. ED Evaluation And Initial Management Pulse oximetry limitations: Standard pulse oximetry is less reliable in sickle cell disease and may miss alveolar hypoxemia; if the patient looks worse than the sat suggests, get an ABG with co-oximetry. Imaging beyond radiography: Lung ultrasound performs well in ACS, with reported sensitivity up to 88-100%, and key findings include B-lines, consolidation, and pleural effusion. Universal antibiotic coverage: All patients with ACS should receive antibiotics because infection triggers about 25% of cases, and atypical coverage belongs in every regimen. Supportive care priorities: Analgesia, incentive spirometry, bronchodilators for wheezing, and careful euvolemia are the backbone of treatment, with fluid overload avoided because it can worsen pulmonary edema. Escalating respiratory support: HFNC or NIPPV can recruit alveoli and reduce the chance of intubation, while invasive ventilation follows standard airway, oxygenation, or ventilation failure criteria. Transfusion strategy decisions: Simple transfusion improves oxygen-carrying capacity, while exchange transfusion lowers the HbS burden for severe or rapidly progressive disease. We walk through the bedside decision points in the chapter. Severe Phenotypes And Important Overlap Rapidly progressive ACS: A distinct high-risk phenotype can progress to respiratory failure within 24 hours and may bring AKI, hepatic dysfunction, altered mental status, or broader multiorgan failure. Predictors of severity: Fever, oxygen saturation under 95%, asthma history, leukocytosis, asplenia, lower baseline hemoglobin, and platelets under 200,000 all point toward a rougher course. Pulmonary embolism overlap: Pulmonary embolism can be the trigger or a concurrent diagnosis in ACS, especially when there is no clear precipitant or the presentation seems out of proportion to the imaging. COVID-associated ACS: COVID-19 raises the risk of pneumonia, pain, and ACS in sickle cell disease, and hypoxic patients should still receive steroids despite rebound vaso-occlusive concerns.

Neuropathic Pain: What Can We Do?

Neuropathic pain is a diagnosis of mechanism, not a synonym for burning or tingling. In the acute care setting, altered sensation on exam and a central-versus-peripheral differential matter more than pain adjectives, and first-line treatment is usually antidepressant-class therapy rather than gabapentin. Diagnosing Neuropathic Pain Central versus peripheral framing: Separating neuropathic pain into central and peripheral causes sharpens the differential, with stroke, spinal cord injury, and multiple sclerosis on one side and diabetic or post-herpetic neuropathy on the other. Pain descriptors alone mislead: Words like burning, tingling, and shooting are not diagnostic; about half of patients with musculoskeletal pain use shooting or tingling language, and roughly 30% describe burning. Sensory exam is pivotal: Neuropathic pain should produce altered sensation over the painful area, making the bedside sensory exam more useful than symptom adjectives or screening questionnaires. Questionnaire limits: Specialized neuropathic pain questionnaires are only about 80% sensitive and specific, so they support but do not replace a history and focused neurologic exam. We get into the bedside distinctions in the episode. High-yield etiologic clues: Post-stroke pain develops in up to 15% of ischemic stroke survivors, and as many as two-thirds of patients with multiple sclerosis develop neuropathic pain, useful context when the complaint is otherwise vague. Treatment Choices in Acute Care Tricyclics as first line: TCAs offer the broadest coverage for neuropathic pain, and the analgesic dose is far lower than the antidepressant dose, with nortriptyline a common starting agent. Duloxetine over gabapentin: Duloxetine is a strong first-line option, especially for peripheral neuropathy, while gabapentin is often prescribed beyond the evidence and generally performs less well than TCAs or serotonergic agents. Pregabalin for narrow syndromes: Pregabalin has better evidence than gabapentin for selected conditions such as diabetic neuropathy and post-herpetic neuralgia, particularly when the diagnosis is narrow rather than broad. Topicals for postherpetic pain: Topical lidocaine is most useful for post-herpetic neuralgia and may be non-inferior to pregabalin, whereas capsaicin can help but is painful to apply. Opioids for short flares: Low-dose opioids can be effective for short-term neuropathic pain flares, with addiction risk likely overstated in carefully selected patients. We cover the caveats on the show. Combination therapy caution: Second-line treatment often means combining first-line agents, but TCAs and SSRIs should not be paired, and tramadol remains a weak choice supported by low-quality evidence.

Lit Matters 2: Immediate Test Result Access Preferred Even by Patients with Abnormal Results

Immediate online release of test results appears to match what most patients want, even when results are abnormal. Early post–Cures Act survey data show higher patient engagement, more early portal messaging, and a clear preference for transparency over delayed clinician-mediated disclosure. Immediate Test Result Access Strong patient preference: Immediate release was favored by 95.7% of surveyed patients, and even among those who perceived results as abnormal, 95.3% still preferred getting them without delay. Abnormal result worry signal: Concern rose when patients thought a result was abnormal, with 16.5% reporting increased worry versus 5% after normal results, but that anxiety rarely changed their preference for immediate access. Engagement after Cures Act: Real-time portal access coincided with a 4-fold increase in patients seeing results before speaking with a clinician and a 2-fold rise in messages during the first 6 hours. Pre-counseling limitation: Advance counseling did not meaningfully reduce worry after result release, suggesting the main issue is not simply preparation but how patients interpret unexpected information. Implementation in the ED: Patient portals are now part of emergency care workflow, so after-visit summaries and expectation-setting need to anticipate that patients may see results before the team does. We get into practical communication tactics in the episode. Survey bias caveat: The sample came from four academic centers and likely overrepresented portal-savvy patients willing to complete surveys, but it remains some of the best current patient-preference data on this policy change.

Sarcoidosis

Sarcoidosis is a multisystem non-caseating granulomatous disease that often hides behind common emergency department complaints. Bilateral hilar adenopathy, lupus pernio, hypercalcemia, and heart block are the high-yield clues, while chronic steroids, cytotoxic agents, and biologics can reshape both presentation and ED treatment. Recognizing Sarcoidosis in the ED Multisystem granulomatous pattern: Sarcoidosis causes non-caseating granulomas that can scar over time, so patients may look well early and later present with pulmonary, ocular, lymphatic, musculoskeletal, or constitutional symptoms. Pulmonary involvement dominance: Pulmonary disease shows up in about 90% of patients, with dyspnea and cough as the usual complaints and bilateral hilar adenopathy as the classic chest x-ray clue. Lupus pernio finding: Lupus pernio is the most specific skin finding: violaceous, shiny nodules on the cheeks, neck, or ears that should immediately raise concern for sarcoidosis. Diagnosis needs tissue: Chest x-ray may be the first hint, but biopsy is needed to confirm sarcoidosis and exclude mimics such as lymphoma. We get into the mimics worth keeping on your radar in the episode. Who gets complicated disease: In the US, sarcoidosis disproportionately affects African Americans and women, with symptom onset usually between ages 20 and 40 and a higher burden of complications in African American patients. Emergency Complications and Management Pearls Cardiac sarcoid red flags: Chest pain or syncope in sarcoidosis should trigger concern for myocarditis, restrictive cardiomyopathy, ventricular irritability, and heart block from granulomas disrupting conduction tissue. Neurosarcoid presentations: Neurosarcoidosis can produce aseptic meningitis, hydrocephalus, seizures, psychosis, or cranial nerve palsies, especially VII, IX, and X, making CT brain and metabolic evaluation reasonable first steps. Hypercalcemia mechanism: Macrophage-driven vitamin D activation can cause hypercalcemia and near-universal hypercalciuria, so stones, abdominal complaints, and psychiatric changes may be the sarcoid clue rather than the diagnosis itself. Medication history matters: Chronic prednisone, methotrexate, azathioprine, mycophenolate, cyclophosphamide, or adalimumab can create immunosuppression, cytopenias, GI toxicity, and drug-interaction problems that change ED decisions. Thrombosis and disposition risk: Sarcoidosis carries a roughly three-fold increased VTE risk, and once ocular, neurologic, cardiac, or hypercalcemic disease appears, many patients need prolonged therapy and a low threshold for admission. We walk through the ED mindset for that disposition call in the chapter.

Keeping Central Lines Sterile

Central line infection prevention starts before the needle: unnecessary central venous catheters should not be placed. For CLABSI prevention, current IDSA and SHEA guidance favors ultrasound-guided insertion, maximal sterile barriers, chlorhexidine skin prep, and subclavian access when feasible. Central Line Sterility Essentials Indication before insertion: The first infection-prevention step is avoiding unnecessary central access; every nonessential catheter carries CLABSI risk and should be removed once it is no longer needed. Training and competency standards: Operator skill is part of sterility, not separate from it; guidelines call for formal education and competency assessment for both inserters and the staff maintaining the line. Subclavian site preference: Subclavian access is the preferred site to reduce infectious complications, a high-evidence recommendation that meaningfully reframes routine site selection in the right patient. Ultrasound and sterile barriers: Ultrasound guidance is recommended alongside maximal sterile barrier precautions, pairing better cannulation practice with lower contamination risk. We get into the practical insertion habits in the episode. Chlorhexidine skin antisepsis: Alcoholic chlorhexidine is the recommended skin prep, and chlorhexidine-containing dressings are favored in patients older than 2 months as part of ongoing CLABSI prevention. What not to do: Two common reflexes do not help: prophylactic antimicrobials are not recommended for short-term or tunneled lines, and routine catheter replacement should not be done.

Lit Matters 3: Safety of High Dose Nitroglycerin Therapy in SCAPE

SCAPE is a hypertensive acute heart failure emergency driven by sudden afterload excess, and early vasodilation is central to treatment. High-dose nitroglycerin appears reasonably safe in severe sympathetic crashing acute pulmonary edema, but the bedside dosing strategy and the role of alternatives like nicardipine remain unsettled. High-Dose Nitroglycerin in SCAPE Afterload-driven physiology: SCAPE is framed as an afterload problem with extreme sympathetic surge, so rapid vasodilation matters more than slow diuresis in the first minutes of care. Hypertensive patient profile: The reviewed cohort was markedly hypertensive at nitroglycerin initiation, with a median systolic pressure of 211 mmHg, reinforcing that these data apply to very high-BP pulmonary edema. Safety signal on hypotension: Hypotension was uncommon despite high-dose nitroglycerin, occurring in 4% of patients, which is the clearest bedside reassurance from this study. Composite outcome caveat: The headline unfavorable outcome was 31%, but that composite included intubation and ICU admission, outcomes that may reflect SCAPE severity more than nitroglycerin toxicity. Dose definition uncertainty: High dose was defined here as at least 100 mcg/min, yet the field still lacks consensus on what initiation rates are safest and most effective. We get into that practice tension in the episode. Alternative vasodilator question: Nicardipine is raised as a potentially better option for some SCAPE patients, a useful reminder that nitroglycerin is not the only afterload-reduction strategy worth considering.