Hippo ERcast March 2023

Intro: VIP Treatment in the ED

VIP treatment exists in emergency departments, whether it is formalized or quietly embedded through professional courtesy, donor status, or a phone call ahead. The real clinical and ethical tension is equity: when special handling protects care and operations, and when it distorts triage, flow, and staff boundaries. VIP Treatment Ethics and Operations Formal versus informal systems: VIP pathways are rarely just a single secret room; they often appear as unofficial prioritization for staff family, donors, EMS, police, or well-connected patients, raising the same equity problem either way. Equity over access: The central issue is not courtesy itself but whether special treatment changes triage, rooming, or disposition for reasons other than medical need, a distinction worth hearing in the episode. Service recovery use: Selective fast-tracking can be defensible as service recovery when it prevents a disruptive waiting-room spiral, but that is different from letting money, fame, or pressure skip the line. Professional courtesy limits: Most claimed VIP status is informal and proximity-based rather than institutional, which is why departments need a clear sense of who, if anyone, gets exceptions and when those exceptions stop. Boundary setting moments: VIP treatment becomes inappropriate when a patient is abusive to ED staff or when accommodations begin to impair departmental flow and other patients' care; we get into the wording in the chapter. VIP care for everyone: A scalable alternative is a universal VIP experience: practice evidence-based medicine, make a clear recommendation, and ask what the patient expects from the visit to align care without favoritism.

ACC Guidelines: The Appetizer (STEMI Equivalents and Troponins)

Acute chest pain evaluation starts with the ECG, and dynamic ischemic changes can outweigh any biomarker shortcut. The 2022 ACC chest pain pathway centers on high-sensitivity troponin I, rapid rule-out only in the right patient, and recognition of STEMI equivalents that should not wait. STEMI Equivalents and ECG Triage Initial ECG priority: The ECG is the first test in suspected ACS, with a 10-minute target from arrival, and an ischemic tracing takes the patient out of any rapid biomarker-only pathway. Dynamic ECG change: Improving or worsening ST-T abnormalities remain concerning for ischemia; even normalization in the ED can represent transient occlusion. We get into why that pattern matters in the episode. Named STEMI equivalents: Posterior STEMI, de Winter pattern, hyperacute T waves, and Sgarbossa or modified Sgarbossa findings should trigger the same urgency as classic ST-elevation. Other high-risk patterns: Wellens pattern, ST elevation in aVR with multilead ST depression, and diffuse ST depression or T-wave inversion signal dangerous proximal or multivessel disease. Prehospital ECG value: EMS ECGs can be enough to activate the cath lab before arrival, especially when they show ischemic changes that later evolve or transiently normalize. High-Sensitivity Troponin and Risk Pathways Assay-specific rule out: Aggressive rapid rule-out pathways apply to hs-cTnI assays, not conventional troponin T or I, so knowing your hospital assay is a patient-safety issue. Rapid rule-out criteria: A single very low hs-cTnI can support ACS rule-out only when symptoms have been present at least 3 hours and the ECG is non-ischemic. Rapid rule-in triggers: An ischemic ECG or hs-cTnI above the 99th percentile is enough to move the patient into an ACS rule-in lane rather than continued low-risk screening. Delta troponin significance: A normal repeat hs-cTnI does not end the workup if the delta is abnormal, because change over time can matter as much as the absolute number. We walk through that nuance in the chapter. HEART score role: HEART remains one of the best predictors of MACE and still supports shared decision-making, even after a patient is ruled out for ACS by a troponin pathway. Type I versus II MI: Type I and Type II MI can produce similar biomarker patterns, but the distinction changes downstream therapy, especially decisions about antithrombotics and cath lab urgency.

Lit Matters 1: Fecal Occult Blood Test

Fecal occult blood testing is a poor rule-in and poor rule-out test for gastrointestinal bleeding in the emergency department. In ED patients with trauma, anemia, syncope, hypotension, or pending anticoagulation or thrombolysis, FOBT rarely changes management and can mislead the workup. FOBT Utility in the ED Poor test performance: FOBT misses many real bleeds: in proven hemorrhagic lesions it was positive only 26% of upper GI bleeds and 57% of lower GI bleeds, making a negative card falsely reassuring. Wrong test in practice: Guaiac testing is designed for spontaneously passed stool under diet and medication restrictions, so the usual ED DRE sample is a less sensitive and often invalid application. False positives and negatives: Red meat, peroxidase-rich vegetables, epistaxis, hemorrhoids, NSAIDs, and anticoagulants can turn cards positive, while intermittent bleeding and vitamin C can hide true blood. Five common bad uses: Routine FOBT for trauma, iron deficiency anemia, syncope, hypotension, or pre-thrombolytic and anticoagulant decisions should be abandoned because it does not reliably direct care. Anemia and shock framing: Iron deficiency anemia still needs endoscopic evaluation, and a tiny amount of occult blood is not a convincing explanation for syncope or hypotension. We get into the bedside implications in the episode. Reasonable narrow exceptions: Selective use remains defensible for invasive infectious diarrhea, where guaiac is 91% sensitive, and for sorting true melena from iron or bismuth stool discoloration.

ACC Guidelines: The Main Course (Decision Pathways)

Acute chest pain workup starts with the ECG, and dynamic ischemic changes trump any rapid troponin pathway. The 2022 ACC chest pain decision pathway centers on high-sensitivity troponin I, fast ED disposition, and separating ACS from non-ACS troponin elevation without over-admitting low-risk patients. ACC Chest Pain Pathway ECG first principle: The ECG is the initial screen for dangerous ischemia, and worsening or even transiently normalizing changes should raise concern rather than reassure. Ischemic ECG findings: STEMI equivalents matter here: Smith-modified Sgarbossa, posterior STEMI, DeWinter pattern, Wellens, and aVR ST elevation with diffuse ST depression all push patients out of rapid rule-out. hs-cTnI requirement: The aggressive ACC rule-out pathways apply only to high-sensitivity troponin I assays, not conventional troponin T or I, so assay-specific cutpoints must be built into your local workflow. Single-sample rule-out: A rapid rule-out is possible with symptoms present at least 3 hours, a non-ischemic ECG, and one very low hs-cTnI, with assay-specific values we walk through in the episode. Rule-in triggers: Rapid rule-in rests on either an ischemic ECG or a hs-cTnI above the 99th percentile, a reminder that biomarkers and tracings both independently move patients into ACS workup. Intermediate troponin pathway: Detectable but nondiagnostic hs-cTnI lives on a continuum, so repeat ECGs and a 2-hour delta troponin become the key next step rather than a binary positive-negative interpretation. Risk Stratification And Next Steps HEART score role: HEART remains one of the best ED predictors of major adverse cardiac events, and ACEP still endorses it even when a troponin pathway has ruled out acute MI. Disposition beyond ACS: A low-risk ACC pathway result supports discharge with a non-ischemic ECG, but it does not erase future MACE risk, so follow-up and risk-factor modification still matter. Prior test reassurance: Recent negative coronary angiography or calcium scoring within 2 years, or a normal functional test within 1 year, meaningfully lowers near-term concern for obstructive disease. Choosing additional testing: Coronary CTA fits patients without known CAD, while stress testing is often favored in known CAD, renal dysfunction, severe contrast allergy, or heavier calcium burden. We get into the practical split in the chapter. Renal dysfunction caveat: Most chest pain decision pathways were not well validated in renal dysfunction, so elevated troponin in this group needs more clinical context than an algorithm alone can provide. Type I versus II MI: Type I MI reflects acute coronary thrombosis, while Type II MI is supply-demand mismatch; the distinction changes downstream decisions on cath lab activation and antithrombotic therapy.

Peds Status Epilepticus

Pediatric status epilepticus is a time-critical neurologic emergency where early benzodiazepines matter and drug effectiveness shifts as seizures persist. Neonatal seizures are often subtle rather than convulsive, with electrolyte derangements and HSV sitting high on the differential. Pediatric Status Epilepticus Approach Early stabilization priorities: Initial management mirrors adult status care: ABCs, monitors, pulse oximetry, bedside glucose, and rapid IV access while treatment starts without waiting for the full workup. First-line benzodiazepine therapy: Benzodiazepines are the clear first-line treatment, with IV lorazepam or diazepam preferred and intranasal or IM midazolam strong options when access is delayed. Receptor shift over time: Ongoing seizures become harder to break because GABA receptors internalize while NMDA activity rises, which is why repeated benzodiazepines lose punch as time passes. Second-line agent choices: Guidelines do not endorse a single best second-line drug; levetiracetam and fosphenytoin are both reasonable, and we get into why many clinicians lean levetiracetam in the episode. Airway and refractory care: Intubation is not treatment failure in prolonged seizures; propofol or thiopental are suggested third-line anesthetic options, with additional rescue nuances discussed in the chapter. Seizure mimic red flags: Dissociative seizures can look dramatic and prolonged, often with flopping movements and vocalization, especially in teenagers with a psychiatric history. Neonates and Special Populations Subtle neonatal seizure signs: Neonatal seizures often lack generalized tonic-clonic activity and instead show eye winking, lip-smacking, or bicycling leg movements that are easy to miss. Electrolyte-driven neonatal causes: In neonates, check glucose plus sodium and calcium early because correctable metabolic problems are common triggers, including hyponatremia from improperly mixed formula. Neonatal first-line therapy: Phenobarbital is first-line for prolonged neonatal seizure, since benzodiazepines are less reliable when neonatal GABA signaling remains relatively excitatory. HSV and structural workup: Head CT matters in neonatal seizure evaluation because vertical HSV and other intracranial pathology belong on the early differential. Genetic epilepsy medication trap: Dravet syndrome and other sodium-channel epilepsies can worsen with fosphenytoin, carbamazepine, or lacosamide, making levetiracetam the safer second-line direction. Infantile spasms clue: Infantile spasms often present as a forward head bob with simultaneous arm flexion and carry a distinctive EEG pattern. We highlight the bedside recognition clue in the episode.

Lit Matters 2: TXA in Non-traumatic Epistaxis

Most non-traumatic anterior epistaxis stops with compression, but persistent bleeding still drives major practice variation in the ED. Topical tranexamic acid appears comparable to lidocaine and epinephrine for getting packed anterior nosebleeds under control, while the basics of pressure, packing, cautery, and coagulopathy reversal still matter most. Topical Therapy for Anterior Epistaxis Compression first principle: Most spontaneous anterior nosebleeds improve with direct pressure alone; the real decision point is the patient who keeps bleeding despite compression and is headed toward topical therapy or packing. Head-to-head topical comparison: In a prospective double-blind randomized trial, topical TXA, lidocaine, and epinephrine had similar bleeding-control times in non-traumatic anterior epistaxis treated with drug-soaked packing. No clear TXA advantage: TXA stopped bleeding in about 9 minutes, essentially matching lidocaine and epinephrine rather than outperforming them as a routine first choice for anterior epistaxis. Side effect signal: Epinephrine did not show the feared systemic blood pressure downside in this study, while the TXA group actually had a slight blood pressure increase. Study population limits: Key exclusions included anticoagulant use, bleeding disorders, and hypertension, leaving open whether the slow-ooze anticoagulated patient is the subgroup where TXA may still matter. We get into that bedside distinction in the episode. Back-to-basics management: When anterior epistaxis persists, fundamentals still carry the case: firm pressure, thoughtful packing, cautery when needed, and reversal of coagulopathy when it is driving the bleed.

High Risk/Low Prevalence: GCA

Giant cell arteritis is an immune-mediated medium-vessel vasculitis where delayed recognition can cost a patient their vision or reveal itself later as aortic disease. Think temporal arteritis in adults over 50 with a new headache, temporal artery changes, jaw claudication, or visual symptoms. Recognizing Giant Cell Arteritis Classic at-risk patient: GCA should move up the differential in adults over 50, especially women and patients with polymyalgia rheumatica, when a new headache appears with temporal artery tenderness or visual complaints. Vision-threatening presentation: Visual symptoms occur in roughly 20% of cases and can range from blurry vision or diplopia to complete monocular vision loss, the complication that makes early treatment urgent. Jaw claudication clue: Jaw claudication is a high-yield bedside clue, and the chewing gum test can reproduce ischemic pain with repetitive chewing. We walk through how to use that pearl in the episode. Classification criteria signal: The American College of Rheumatology criteria reach about 93% sensitivity and 91% specificity when 3 of 5 features are present, including age over 50, new headache, temporal artery abnormality, ESR elevation, and biopsy findings. High-stakes complications: Untreated disease is not just about headache and vision loss; first-order aortic branch involvement is common, and stroke or TIA clusters early after diagnosis. Diagnosis and Emergency Management Inflammatory markers together: ESR and CRP are more useful together than alone, but normal markers do not exclude early GCA and platelet elevation may add diagnostic weight. Biopsy versus ultrasound: Temporal artery biopsy remains the reference standard, yet its sensitivity is imperfect and vascular ultrasound is increasingly used as a noninvasive confirmatory test. Steroids before confirmation: When suspicion is meaningful, start glucocorticoids before confirmatory testing; prednisone 60 mg daily is the headline outpatient regimen for less severe presentations. Severe symptom escalation: Vision loss or other major ischemic features call for methylprednisolone 1000 mg IV and admission, with additional disposition nuances we get into in the chapter. Follow-up determines disposition: Patients without severe features may go home only if close follow-up is reliable, ideally coordinated with primary care and rheumatology while confirmatory testing is arranged.

When I intubate, I don't just VL, I VL 2.0.

Videolaryngoscopy is no longer one technique. Hyperangulated blades and Mac-style video blades create different views, require different tube-delivery strategies, and fail in different ways during emergency airway management. Videolaryngoscopy 2.0 Airway Approach Precise VL terminology: “VL” is too vague for modern airway practice; naming hyperangulated VL versus Mac-VL better describes the intubation you actually performed and improves how clinicians communicate about difficult airways. Blade geometry matters: The key distinction is blade shape, not the presence of a camera: hyperangulated blades run about 60 to 70 degrees, while Mac-VL keeps standard Macintosh geometry with a very different feel and workflow. Different device techniques: Hyperangulated VL generally needs a rigid stylet for tube delivery, whereas Mac-VL is better suited to bougie-assisted intubation and should not be approached with the same hand mechanics. Soiled airway advantage: Mac-VL can look past the tongue and still permits a direct view if blood or vomit obscures the screen, a practical rescue advantage we get into in the episode. Teaching and backup planning: Mac-VL is useful for teaching direct laryngoscopy while sharing the screen, but neither blade guarantees first-pass or rescue success, so a backup airway plan still has to be explicit. Research language problem: Pooling hyperangulated devices and Mac-VL under one “VL” label muddies airway research, because device geometry changes performance, complications, and what success rates really mean.

Lit Matters 3: CT sensitivity for pyogenic spinal infections

Pyogenic spinal infection is an ED back-pain diagnosis that CT often misses, especially spinal epidural abscess. In patients already concerning enough to undergo MRI, CT was reasonably sensitive for infections outside the canal but performed poorly for SEA, making MRI the imaging test of choice when suspicion is real. CT Versus MRI for Spinal Infection MRI first-line imaging: Pyogenic spinal infection remains an MRI diagnosis in emergency care; when clinical concern is meaningful, starting with CT risks false reassurance and delayed recognition of epidural disease. CT sensitivity gap: CT detected 79% of pyogenic spinal infections overall in masked review, but that headline number hides the main problem: performance collapsed for spinal epidural abscess. SEA detection failure: Spinal epidural abscess was seen on CT only 18% of the time, reinforcing that a negative CT does not come close to excluding the highest-stakes spinal canal infection. Outside-the-canal infections: CT was better for vertebral, disc, paravertebral, and other extra-canal disease, reaching 83% sensitivity for infections outside the spinal canal, a distinction worth hearing in the episode. Initial read limitations: Real-world first reads underperformed the study overread, with just 50% overall sensitivity, which matters far more at 2 a.m. than idealized retrospective image review. Clinical Pattern of Pyogenic Spinal Infection Overlapping infection syndromes: Pyogenic spinal infections commonly travel together rather than appearing in isolation; finding one lesion should immediately raise concern for a second spinal infectious focus. SEA co-infection signal: Most spinal epidural abscess cases were accompanied by another spinal infection, with 82% of SEA patients having an associated lesion somewhere else in the spine. Paravertebral abscess association: Paravertebral abscess or infection tracked especially closely with epidural disease: every patient with PVA in this cohort also had a spinal epidural abscess. Septic facet warning: Septic facet joint infection is uncommon but not benign; more than 20% of patients with septic facet infection also had a spinal epidural abscess. Whole-spine implications: Noncontiguous lesions are part of the concern once one spinal infection is identified, though the practical MRI extent questions and ED tradeoffs are where we get into nuance in the episode.