Hippo ERcast February 2026

February ERcast Intro 2026

Emergency care is a team sport, and high-performing EDs depend on more than physician decision-making alone. ERcast is shifting toward a broader emergency medicine lens that pairs clinical excellence with the communication, leadership, and workflow realities of nurses, APPs, EMS, techs, and the wider ED team. ERcast Clinical Perspectives Transition Team-based emergency care: Emergency medicine works best as a coordinated team effort, and the new direction centers bedside care delivered across physicians, nurse practitioners, nurses, EMS, techs, and other ED roles. Clinical continuity commitment: The core promise remains high-yield emergency medicine grounded in clinical excellence, current guidelines, and practical bedside relevance despite the name change and host transition. Expanded ED viewpoints: The broader format moves beyond a physician-only lens to highlight how different team members see the same resuscitation, handoff, and operational problems. We get into that wider perspective in the episode. Leadership and communication focus: Strong emergency care depends on leadership, communication, and other nontechnical skills that shape safety, flow, and team function as much as medical knowledge does. Host transition plan: Brett Murray, an emergency physician, and Anne Steckowych, a nurse practitioner, step in as new hosts while Drew and Andy remain involved through the transition period.

Cavernous Sinus Thrombosis with Brit Long

Cavernous sinus thrombosis is a rare but vision- and life-threatening cause of headache, fever, and painful ocular findings after facial, sinus, or dental infection. The diagnosis turns on recognizing cranial neuropathies early, getting contrast imaging fast, and starting broad-spectrum therapy before complications spread bilaterally. Recognizing Cavernous Sinus Thrombosis Venous outflow obstruction: CST is a thrombophlebitic process in the cavernous sinus that raises venous pressure, impairs orbital drainage, and produces cranial neuropathies rather than a simple localized skin infection. Classic symptom cluster: The bedside pattern is headache, fever, and ocular abnormalities such as chemosis, proptosis, ptosis, or ophthalmoplegia, with headache present in about 90% of cases. Abducens nerve vulnerability: CN VI palsy is the most common cranial nerve finding, so limited eye abduction or a lateral rectus palsy should sharply raise concern for cavernous sinus involvement. Rapid bilateral progression: Because the cavernous sinuses communicate across the midline, unilateral orbital findings can progress to both eyes within 48 hours. We get into the bedside pattern recognition in the episode. Infectious source patterns: Septic CST usually follows sinusitis or facial infection, with Staphylococcus aureus causing roughly 70% of cases; dental and other head-and-neck sources matter too. Diagnosis and Initial Management Clinical diagnosis first: Normal or nonspecific labs do not exclude CST; blood cultures are positive in about 70%, but the diagnosis still rests on history, exam, and urgent imaging. Emergency department imaging: CT head and orbits with IV contrast and delayed-phase imaging is the practical first-line ED study, looking for filling defects, venous congestion, and sinus wall bulging. MRV sensitivity advantage: MR venography is the most sensitive test, around 95%, and becomes especially important when CT is unrevealing but the clinical picture still fits. Empiric antimicrobial backbone: Initial treatment centers on broad-spectrum IV antibiotics, typically pairing vancomycin with ceftriaxone or cefepime, with metronidazole added for dental or sinus sources. Anticoagulation uncertainty: Anticoagulation is considered case by case because evidence is limited, with potential benefit against clot propagation but hemorrhage and selection questions still requiring specialist input. We walk through that decision tension in the chapter.

Lit Matters 1: DASA Score at ED Triage

Emergency department workplace violence is common, costly, and hard to anticipate at triage. The Dynamic Appraisal of Situational Aggression score is a 7-item, 120-second screen that proved feasible across five EDs, but outcome benefit and bias remain the central unanswered questions. DASA Score at ED Triage Rapid triage screening tool: DASA is a 7-item aggression-risk screen that takes about 120 seconds and was embedded directly into Epic, making it practical for routine triage workflow in a large mixed academic-community ED system. System-wide feasibility signal: Triage nurses assigned a DASA score in more than 80% of adult encounters across 192,947 visits, a strong implementation signal for real-world ED use. We get into what likely made uptake work in the episode. Risk strata at a glance: Scores were grouped as low risk at 0, moderate at 1 to 3, high at 4 to 5, and imminent risk above 5, giving teams a shared language for situational aggression at the bedside. Who scored higher: Higher-risk scores clustered with male sex, younger age, higher ESI acuity, and arrival by police, ambulance, or air, with police arrival showing the strongest association. Bias and validity concern: Black race was associated with higher scores, raising a major concern that any operational value could come bundled with racial bias unless prospective validation addresses it directly. Feasible not outcome-proven: This was a descriptive single-system study, so it supports feasibility and pattern recognition but does not show fewer assaults, safer staff, or better patient outcomes after DASA implementation.

How an OB/GYN Approaches Chronic Pelvic Pain

Chronic pelvic pain is usually multifactorial, and endometriosis is only one part of the differential. In the ED, the high-value move is to exclude ovarian torsion, ectopic pregnancy, and tubo-ovarian abscess, then use a careful history and targeted pelvic exam to separate gynecologic from myofascial pain. ED Approach to Chronic Pelvic Pain Broad differential diagnosis: Chronic pelvic pain means abdominopelvic pain causing distress or dysfunction for more than 3 to 6 months, with common causes including dysmenorrhea, pelvic floor myalgia, vestibulodynia, interstitial cystitis, and endometriosis. Dangerous diagnoses first: Before labeling pain as chronic, rule out ovarian torsion, ectopic pregnancy, and tubo-ovarian abscess, especially when the current episode is new, different, or clearly escalating. Pattern-based pain history: Pain quality, cyclicity, baseline pain with flares, and triggers such as intercourse, bowel movements, position, or heating pads often narrow the source faster than a broad undirected review of symptoms. Musculoskeletal pain clues: A sensation that something is falling out can point to levator pain, while pain shooting down the back of the leg or wrapping like a belt suggests piriformis or other pelvic floor involvement. Targeted abdominal screening: Start with the back and abdomen before the pelvic exam; scoliosis, prior surgical scars, and a positive Carnett sign can shift suspicion toward abdominal wall or musculoskeletal pain. We get into how that changes the exam sequence in the episode. Expectation setting early: Set up chronic pelvic pain care as a multimodal process rather than a one-visit diagnosis, because early validation and a concrete follow-up plan can keep patients from falling through the cracks. Pelvic Exam Pearls and Initial Treatment Single-digit bimanual technique: Using one finger instead of two during the bimanual exam often improves comfort and cooperation without sacrificing useful information in a patient already sensitized by pain. Judicious speculum use: A speculum exam is not mandatory in every chronic pelvic pain evaluation; reserve it for situations where it will answer a specific question rather than reflexively adding another painful step. Systematic pelvic floor exam: Pressing the levator plate at the 5 and 7 o'clock positions and the obturator internus at 3 and 9 o'clock helps identify reproducible myofascial pain before moving to cervix, uterus, and adnexa. Internal versus external tenderness: Pain that is mainly internal raises concern for an adnexal source, while pain provoked more by external abdominal hand pressure points toward a muscular disorder. That bedside distinction is worth hearing in the chapter. Ultrasound for endometriosis clues: Pelvic ultrasound can help when endometriosis is suspected, particularly if an endometrioma is on the table, but a normal scan does not settle the broader chronic pelvic pain workup. First-line symptom treatment: NSAIDs, muscle relaxants, pelvic floor physical therapy, and hormonal therapy such as oral contraceptives are common starting points, with SNRIs, tricyclics, or gabapentinoids sometimes used to turn down pain amplification.

Lit Matters 2: IM Epinephrine for Anaphylaxis – 0.3 mg vs 0.5 mg

Adult anaphylaxis is often undertreated, and fixed 0.3 mg IM epinephrine may underdose many patients over 50 kg. In this retrospective ED cohort, an initial 0.5 mg IM dose was associated with less escalation of care and no clear increase in short-term safety events. IM Epinephrine Dose in Adult Anaphylaxis Weight-based dosing gap: Guidelines target 0.01 mg/kg IM up to 0.5 mg, so many adults over 50 kg likely receive less than intended when treatment defaults to a 0.3 mg autoinjector. Escalation of care signal: Initial 0.5 mg IM epinephrine was linked to markedly fewer escalations within 6 hours than 0.3 mg, with less need for repeat epinephrine, infusion, or intubation. Early symptom resolution: Symptom resolution after the first dose was higher with 0.5 mg, suggesting the larger adult dose may better match the physiologic target in typical ED patients. Short-term safety findings: Peak heart rate, blood pressure change, ischemic ECG findings, arrhythmia, and troponin abnormalities were not clearly worse with 0.5 mg in adults. We get into the safety caveats in the episode. Practice-changing implication: For adults with anaphylaxis, this study strengthens the case that 0.5 mg IM should be the routine starting dose rather than 0.3 mg, especially when body weight exceeds 50 kg. Autoinjector mismatch problem: Available autoinjector sizes still lag behind ideal adult dosing, creating a real-world gap between guideline-based treatment and what many patients actually receive.

Myxedema Coma in the ED

Myxedema coma is decompensated severe hypothyroidism marked by altered mental status, hypothermia, and bradycardia. In the ED, the diagnosis is often missed because early symptoms are nonspecific, while treatment hinges on supportive care, thyroid hormone replacement, and finding the precipitating trigger. Recognizing Myxedema Coma Classic triad recognition: Altered mental status, hypothermia, and bradycardia are the bedside trio that should immediately raise concern for myxedema coma, especially in an older patient with known hypothyroidism. Early symptom pattern: Fatigue, activity intolerance, and persistent cold intolerance often precede collapse, making a careful symptom timeline and medication history more useful than the initial complaint suggests. High-risk patient profile: Untreated hypothyroidism, recent medication interruption, and elderly patients dependent on others for pill administration are recurring setup factors for this presentation. Precipitating stressors: Infection, trauma, surgery, cold exposure, and sedatives or narcotics can tip compensated hypothyroidism into myxedema coma. We get into the common ED trigger patterns in the episode. ED Workup and Initial Management Core diagnostic studies: TSH, free T4, cortisol, electrolytes, glucose, CBC, CMP, ABG, and infection screening frame both the diagnosis and the metabolic complications that often drive instability. Electrocardiographic clues: Bradycardia, low voltage, and QT prolongation are the ECG findings that fit severe hypothyroidism and help explain hemodynamic fragility in the sickest patients. Supportive care priorities: Initial management starts with ABCs, cautious fluids for hypotension, and gentle rewarming, because aggressive volume loading or rapid warming can worsen an already unstable physiology. Hormone and steroid therapy: IV levothyroxine is the cornerstone of definitive treatment, and hydrocortisone is commonly paired early while adrenal insufficiency is still in the differential. Escalation decisions: Refractory hypotension may require vasopressors, severe bradycardia can push pacing discussions, and some patients need ICU transfer for replacement and monitoring nuances we cover in the chapter.

The Crashing Asthmatic

Severe asthma is an airway-obstruction problem where fatigue, rising CO2, and dynamic hyperinflation matter more than a pulse-ox number alone. Hypoxemia in asthma is a red flag, and post-intubation harm often comes from the ventilator rather than the laryngoscopy. Recognition and Initial Severe Asthma Care Hypoxemia as danger sign: A hypoxic asthmatic is very sick because isolated bronchospasm should not cause much oxygen failure; subtle distress usually appears earlier as tripod posture, large tidal volumes, and accessory muscle use. BiPAP for work of breathing: Any increased respiratory effort is a reason to start noninvasive ventilation, paired with continuous albuterol to unload the respiratory muscles before fatigue wins. We get into the bedside coaching nuances in the episode. Albuterol as core therapy: Beta agonists remain first-line and the practical stance is aggressive dosing; albuterol-related lactate can rise without meaning occult shock if the rest of the picture fits asthma. Steroids without route drama: Glucocorticoids are foundational, and oral and IV steroids have nearly identical onset and effectiveness, so route choice usually follows access and patient tolerance rather than potency. Adjuncts after the basics: Magnesium and ketamine can help as add-on therapies, but they are not the first move; getting albuterol, steroids, and positive pressure right is what usually turns the patient around. Intubation and Ventilator Management Fatigue and acidosis triggers: Intubation decisions hinge on fatigue and respiratory acidosis: an asthmatic should be alkalotic from high minute ventilation, so a drifting CO2 or hypercapnic encephalopathy is ominous. Fast tube slow breaths: The intubation principle is simple: place the tube quickly with your most experienced operator, then ventilate slowly because rapid rescue ventilation worsens air trapping rather than fixing acidosis. Initial ventilator strategy: Severe asthma needs prolonged exhalation, so start around 10 breaths per minute and favor enough tidal volume to shorten inspiratory time; the bedside setup details are worth hearing in the chapter. Flow waveform as monitor: The key ventilator check is whether expiratory flow returns to zero before the next breath; failure means dynamic hyperinflation with rising intrathoracic pressure, hypotension, and possible arrest. Auto-PEEP rescue move: When peak pressures climb and alarms cascade, disconnecting from the ventilator and helping the chest exhale is the first rescue step, then reduce respiratory rate and recheck auto-PEEP and plateau pressure. Permissive acidemia and sedation: Deep sedation is often necessary to prevent dyssynchrony, and permissive acidemia is acceptable in severe asthma; bicarbonate is generally unhelpful because it generates more CO2 to exhale.

Lit Matters 3: STAMP Score for PE Risk

Intermediate-high-risk pulmonary embolism can decompensate within 48 hours despite normal blood pressure at presentation. The STAMP score is a bedside risk tool for short-term PE deterioration that combines syncope, RV dysfunction, age, MAP, and chest pain into a simple early-stratification framework. STAMP Score for Intermediate-High-Risk PE Early decompensation window: Intermediate-high-risk PE is not benign; about 10% deteriorate early, making the first 48 hours the key monitoring period for patients with RV strain and positive biomarkers. Five-item bedside model: STAMP uses five readily available variables: syncope, chest pain, age 65 or older, mean arterial pressure, and the TAPSE-to-PASP ratio as the echo marker of RV dysfunction. RV dysfunction signal: A TAPSE/PASP ratio of 0.33 or less identifies impaired RV-PA coupling and was one of the strongest predictors of short-term clinical worsening in this cohort. Risk tier separation: The low-risk STAMP group had 0% 48-hour deterioration in both derivation and validation cohorts, while adverse events clustered in the intermediate and high tiers. Validation performance: The validation cohort showed an AUC around 0.85, suggesting good discrimination for early PE decompensation. We get into what that does and does not justify in the chapter. Disposition uncertainty: STAMP may help frame ICU versus floor discussions in intermediate-high-risk PE, but the action thresholds and escalation decisions still need broader external validation.