Hippo ERcast June 2023

EM - We Have a Problem

Emergency medicine is under visible workforce and sustainability strain, with boarding, staffing limits, and post-pandemic attrition colliding with a collapse in Match fill rates. The 2023 EM Match left 555 positions unfilled at 131 programs, turning a long-building narrative problem into a specialty-wide credibility crisis. Emergency Medicine Workforce Crisis Match collapse signal: Unfilled emergency medicine residency spots jumped from roughly 30 in prior cycles to 219 in 2022 and 555 in 2023, a stark marker that the specialty’s recruitment problem is no longer theoretical. Workforce projection fallout: The 2021 ACEP workforce study projected a surplus of 7,000 to 13,000 emergency physicians by 2030, and even critics of the model agree the narrative damage has outlived the paper itself. Residency expansion pressure: New EM programs and expansion of existing residencies widened the gap between training positions and applicant interest, with smaller or newer programs facing the greatest vulnerability. Operational stressors stack: Boarding, overcrowding, staffing shortages, and shifting performance metrics have compounded the burnout left by a two-plus-year pandemic, creating a plain sustainability problem at the bedside. Turnover beyond physicians: Retention problems are not limited to attendings; APP turnover is part of the same workforce instability, adding another layer to coverage, culture, and continuity concerns in the ED. Fragmented specialty messaging: Emergency medicine’s public narrative is diluted when major organizations send conflicting signals about workforce, training, and scope. We get into why that matters in the episode.

EEM Fest Cardiogenic Shock: Pitfalls to Avoid

Cardiogenic shock is a low-perfusion emergency where hypoxemia, high work of breathing, and pump failure can spiral quickly. Early noninvasive ventilation, bedside ultrasound volume assessment, norepinephrine support, and rapid cause-finding are the core moves in emergency management. Cardiogenic Shock Initial Management Early NIPPV strategy: High work of breathing worsens myocardial oxygen demand, so noninvasive ventilation is the first stabilizing move; starting around EPAP 5 cm H2O can unload the patient without stealing too much preload. Pre-intubation stabilization: If possible, resuscitate before intubation because induction can precipitate collapse in severe cardiogenic shock. We get into the practical airway sequencing in the episode. POCUS volume assessment: Bedside ultrasound is the key fork in the road: a full IVC and loaded RV push you toward pressure support, while a flat IVC can justify cautious 250 mL fluid boluses. Mottling as red flag: Cool mottled extremities are a poor prognostic sign and a bedside clue to inadequate end-organ perfusion, even before labs fully declare how sick the patient is. Norepinephrine first pressor: Norepinephrine is the blood-pressure workhorse in cardiogenic shock, with a practical target of at least MAP 60 while you confirm the physiology and organize definitive treatment. Arterial line accuracy: Peripheral vasoconstriction makes cuff pressures unreliable in shock, so an arterial line gives cleaner hemodynamics and safer titration when vasoactive support is changing quickly. Finding The Cause And Escalating Support Ischemia as leading cause: Acute cardiac ischemia drives roughly 75% of cardiogenic shock, making aspirin, antiplatelet therapy, anticoagulation, and especially early PCI the highest-yield cause-directed priorities. Sepsis overlap physiology: Septic and cardiogenic shock can coexist, so if infection is plausibly on the table, send cultures early and start broad-spectrum antibiotics rather than anchoring on a single phenotype. Diuresis timing caution: Pulmonary edema does not automatically mean early diuresis; the hypotensive patient in cardiogenic shock often cannot tolerate it until perfusion is restored. Dobutamine perfusion endpoints: Dobutamine is for persistent low-output signs despite an acceptable MAP, but it can drop blood pressure; titrate to perfusion markers like urine output, mental status, and lactate trend. Mechanical bridge options: IABP, LVAD, and ECMO are bridge therapies when standard measures are failing, with ECMO showing a possible mortality benefit in selected patients. We cover where these fits start to matter on the show.

Lit Matters #1: Use of Neuroimaging for Patients with Dizziness in Outpatient Clinics vs Emergency Departments

Head CT has poor sensitivity for posterior fossa stroke in dizzy patients, and neuroimaging for dizziness is common despite a low diagnostic yield. In U.S. claims data, emergency departments image far more often and earlier than outpatient clinics, with MRI driving most of the spending. Dizziness Neuroimaging in Emergency Care Low-yield imaging pattern: Neuroimaging for dizziness was obtained within 6 months in 35% of ED visits versus 15% of outpatient presentations, a large practice gap that raises real value and overuse concerns. Same-day ED scanning: ED patients were usually imaged the same day, while clinic patients were scanned around day 10, highlighting how setting strongly shapes both testing intensity and timing. CT sensitivity problem: Noncontrast head CT is a weak rule-out test for posterior fossa infarct, with about 16% sensitivity, so a normal scan can falsely reassure clinicians facing possible central vertigo. MRI limits and cost: Diffusion-weighted MRI is substantially better for ischemia detection, around 83% for posterior fossa infarct, yet early studies can still miss small strokes and MRI accounts for most spending. Who merits concern: Central causes cluster in dizziness with neurologic features such as gait instability, visual symptoms, focal sensory or motor deficits, or sudden hearing loss. We get into the bedside red flags in the episode. HINTS exam caution: The HINTS exam can outperform early imaging in the right hands, but misapplication is common outside true acute vestibular syndrome, making indiscriminate use a setup for error.

Go Ahead & Brush Your Shoulder Off: Thoracic Outlet Syndrome in the ED

Thoracic outlet syndrome is a compression disorder of the brachial plexus, subclavian vein, or subclavian artery that is often missed early in the ED. Neurogenic disease causes pain and paresthesias, while vascular disease can present with arm swelling, limb ischemia, stroke, or pulmonary embolism. Thoracic Outlet Syndrome Recognition Three-compartment compression anatomy: TOS arises where the neurovascular bundle is crowded at the scalene triangle, costoclavicular space, or beneath the pectoralis minor, a useful frame for otherwise scattered shoulder, arm, and vascular complaints. Neurogenic versus vascular patterns: Neurogenic TOS is most common and points to C8-T1 symptoms, neck or shoulder pain, and hand weakness, while venous or arterial disease shifts the picture toward edema, cyanosis, claudication, or ischemia. Swollen arm red flag: Venous TOS is the form that produces true unilateral arm swelling and heaviness from subclavian vein compression, a pattern worth separating from cellulitis, DVT, or musculoskeletal shoulder pain. Ischemic complication spectrum: Arterial TOS can present with pallor, cold intolerance, distal embolic symptoms, and even stroke, underscoring why missed vascular disease is more than a chronic pain diagnosis. We get into the bedside consequences in the episode. Gilliatt-Sumner hand finding: Thenar or hypothenar wasting, the classic Gilliatt-Sumner hand, is a high-credibility clue to chronic neurogenic TOS rather than a routine overuse complaint. Exam, Imaging, and Disposition Provocative bedside maneuvers: Roos, Adson, and Wright testing can support the diagnosis when they reproduce pain, paresthesias, pallor, cyanosis, or pulse change, but none should be treated as a stand-alone rule-in test. Roos test signal: The elevated arm stress test is commonly abnormal in TOS; inability to complete the maneuver because of worsening symptoms is more concerning than simple forearm fatigue. Vascular imaging pathway: Suspected venous TOS starts with venous ultrasound, while arterial disease pushes toward Doppler studies, angiography, or CT angiography in a position that can reveal dynamic compression. Conservative first-line care: Most neurogenic cases begin with physical therapy and symptom control using agents such as ibuprofen or muscle relaxants, while vascular thrombosis changes the urgency and trajectory of care. Admission and consultation triggers: Ischemia, venous or arterial thrombosis, aneurysm, stenosis, or intractable pain should prompt admission and vascular surgery involvement, with thrombolysis and decompression reserved for selected cases. We walk through where the ED handoff matters in the chapter.

Clinical Decision Rules are Ruining Medicine

Clinical decision rules often look more objective than they are, and many were adopted before they proved they improved real-world care. For pulmonary embolism, pediatric trauma, chest pain, and C-spine clearance, the key question is simple: does the rule outperform usual practice and clinical judgment alone? Why Decision Rules Mislead Four-step evidence pathway: A rule is not ready for routine use after derivation alone; it should survive validation, external validation, and an implementation study showing better care, not just cleaner statistics. Implementation study standard: The most important test is whether clinicians using the rule improve outcomes or resource use versus clinicians not using it, a step very few decision rules ever reach. False objectivity problem: Scores can look precise while depending on subjective inputs, so two clinicians may generate different numbers and still have the result treated as if it were hard fact. Zero-miss culture pressure: Many rules are built around near-100% sensitivity, a design goal that predictably drives overtesting and can turn rare misses into the dominant standard of care. Shared decision-making loss: Binary positive-or-negative rules often replace bedside judgment with cookbook medicine and make nuanced risk conversations harder. We get into that cultural shift in the episode. Rules Worth Trusting More PERC and YEARS for PE: For pulmonary embolism, PERC and the YEARS algorithm are among the few tools backed by controlled implementation data showing they can improve practice rather than just classify risk. Canadian C-spine advantage: Canadian C-spine has both external validation and implementation evidence, with 99.4% sensitivity and a 9% absolute reduction in imaging in a cluster trial. Population matters most: Even strong rules can fail when moved into lower-risk settings, so trauma-room performance should not be assumed to hold in fast track or community populations. Learning from likelihood ratios: A practical use for rules is educational: inspect which variables carry the strongest likelihood shifts and compare them against your own gestalt. We walk through that approach in the chapter. Common Rules That Underperform Ottawa ankle limits: Ottawa Ankle was validated, but outside Ottawa it increased x-ray use in a multicenter study, and a narrow rule-based exam can miss injuries elsewhere in the ankle. PECARN head tradeoff: PECARN head injury has near-100% sensitivity, but compared with clinical judgment it has much lower specificity, meaning more children get scanned while the same injuries are missed. PECARN abdominal uncertainty: The pediatric blunt abdominal injury rule has external validation but no implementation study, and its low specificity raises concern for more CT use in community settings. HEART score mismatch: HEART was built for simplicity rather than calibrated risk, creating odd equivalences such as age 50 carrying the same points as a positive troponin. Judgment versus checklist: The recurring test is whether a rule beats what experienced clinicians already do at the bedside; for several popular tools, the answer appears to be no.

Lit Matters #2: Triage End-tidal Carbon Dioxide vs Standard Vital Signs

Low end-tidal carbon dioxide at ED triage is a stronger early warning sign for in-hospital mortality and ICU admission than standard vital signs alone. In undifferentiated emergency patients, ETCO2 appears to track illness severity through acidosis and poor perfusion better than pulse, blood pressure, respiratory rate, or oxygen saturation. Triage End-tidal CO2 Risk Stratification Low ETCO2 signal: A low triage ETCO2 was the clearest abnormality linked to bad outcomes, with non-survivors clustering around 22 mmHg versus about 35 mmHg in survivors. Outperforming standard vitals: ETCO2 beat every routine triage vital sign for predicting both mortality and ICU admission, with mortality discrimination reaching an AUC range of 0.82 to 0.88. Useful rule-out profile: An abnormal ETCO2 threshold carried a negative predictive value of 99% for mortality, making it most attractive as an early reassurance tool when the number is normal. Perfusion and acidosis link: The physiologic signal is probably downstream of poor perfusion and metabolic acidosis, supported by correlations with lactate, bicarbonate, and anion gap. Normal versus abnormal framing: The practical bedside takeaway is to treat ETCO2 like another vital sign: normal is reassuring, abnormal deserves attention, and the exact cut points are worth hearing in the episode. Gestalt comparison gap: What this study still does not answer is whether ETCO2 adds value beyond an experienced triage nurse or physician's first-look gestalt.

Feel the Burn: An Evidence Based Approach to Rhabdomyolysis

Rhabdomyolysis is skeletal muscle necrosis that can rapidly progress to acute kidney injury, especially after trauma, crush injury, ischemia-reperfusion, or extreme exertion. Diagnosis hinges on the right clinical context plus a characteristic lab pattern, and early management is primarily thoughtful fluid resuscitation rather than bicarbonate or dialysis by default. Recognizing Rhabdomyolysis Early High risk patient groups: Suspect rhabdomyolysis after crush injury, major muscle trauma, vascular compromise with reperfusion, or metabolic stressors such as strenuous exercise, toxins, infections, and inherited myopathies. Classic bedside features: Muscle pain, weakness, swelling, and tea-colored urine are the classic clues, but the bigger pearl is a low threshold for testing when the history fits, especially in older patients with limited reserve. Core laboratory pattern: Creatine kinase above 5 times the upper limit of normal or above 1000 IU/L supports the diagnosis, often alongside rising creatinine, hyperkalemia, elevated AST, LDH, and urine myoglobin. CK trend timing: CK usually peaks at 24 to 72 hours, so serial values matter more than a single number. We get into the practical timing for when trending adds value in the episode. AKI Prevention And Complications Primary management target: Acute kidney injury is the complication to prevent first, and initial treatment centers on isotonic crystalloid with Lactated Ringer's or saline rather than reflex adjuncts. Fluid strategy basics: A starting infusion rate around 400 mL per hour is a reasonable anchor, with resuscitation titrated to urine output and often measured with a Foley for accuracy. Bicarb and diuretic limits: Despite common teaching, current evidence does not support bicarbonate or diuretics for routine prevention or treatment of rhabdomyolysis-associated AKI, a nuance we unpack in the chapter. Electrolyte danger zone: Hyperkalemia is the electrolyte abnormality that can kill early through dysrhythmia, while hyperphosphatemia and hypocalcemia also demand careful, complication-aware management. Dialysis decision point: Renal replacement therapy has no proven role in preventing AKI in rhabdomyolysis; use it for standard AKI indications based on renal impairment and the overall clinical picture. Complication surveillance: AKI is the most common systemic complication, but early and late morbidity also includes fluid overload, hepatic or cardiac dysfunction, DIC, and compartment syndrome. Risk Stratification And Prognosis McMahon score role: The McMahon score uses admission demographics and routine labs to predict risk better than CK alone, particularly for renal replacement therapy and severe outcomes. Meaningful prognostic cutoff: A McMahon score of 6 or higher marks a higher-risk patient, though the score is more useful for prognosis than for dictating a completely separate treatment pathway. Limits of CK alone: CK helps confirm muscle injury, but it is less specific than the McMahon score for forecasting who will progress to dialysis-level kidney failure. Guideline anchored approach: The AAST consensus gives a practical framework for diagnosis, fluid choice, electrolyte management, and when prognostic tools help without overcalling their bedside authority.

Lit Matters #3: Sleep and Fatigue Risk in EM Physicians

Emergency physicians spend a meaningful share of clinical time in fatigue states associated with impaired performance and higher error risk. Wearable sleep data suggest the signal is not limited to nights: later shift starts, especially afternoons, may carry circadian penalties, while individual variation appears to matter even more. Sleep and Fatigue in EM Fatigue exposure on shift: Emergency physicians spent about 25% of work periods in lower readiness states, a level associated with impaired performance and elevated risk of error rather than simple end-of-shift tiredness. Average sleep duration: Mean sleep time was 6.77 hours per day, below the usual 7 to 9 hour adult target, reinforcing that baseline sleep debt may be built into routine emergency practice. Poor sleep quality signal: Sleep quality averaged 7.71 on a 10-point scale where lower is better, pointing to fragmented, less restorative sleep even when total sleep time looked only modestly reduced. Later shift circadian effect: Later shift starts were linked to slightly lower readiness scores, with afternoon starts showing a concerning signal that challenges the usual focus on overnight work alone. We get into that nuance in the episode. Individual variation dominates: Between-physician differences in readiness were much larger than the effect of shift start time, suggesting personal sleep vulnerability and scheduling fit may matter more than any single roster rule.