An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Bronchitis
Acute bronchitis is usually viral and self-limited, but pneumonia, asthma, COPD exacerbation, and pertussis can require different management. Unnecessary antibiotics create adverse effects, resistance, and false reassurance without shortening typical illness.
A 34-year-old teacher sits forward on the stretcher, coughing hard enough to bring tears to her eyes. For 10 days, the cough has shifted from dry and irritating to productive of scant yellow sputum; she has no measured fever but feels “worn out.” Her lungs have scattered rhonchi that partially clear with coughing, and her oxygen saturation is 98% on room air. The question is whether this is a self-limited airway illness—or the pneumonia that cannot be missed.
— What’s your move? Read on.
Before you read
When do antibiotics help, and when do they only cause harm?
Which symptomatic treatments have meaningful benefit?
When to Think of It
Acute cough, usually lasting 1–3 weeks, with or without sputum, after an upper-respiratory prodrome; rhonchi or wheeze may be present. Colored sputum does not reliably indicate bacterial infection.
Sick or Not Sick
The key fork is pneumonia versus uncomplicated bronchitis. Assess vital signs, oxygenation, work of breathing, focal lung findings, mental status, and comorbidity; chest imaging is indicated when pneumonia is clinically plausible, not automatically for every cough.
The First Fifteen Minutes
Hypoxemia or respiratory distress → oxygen by nasal cannula 1–6 L/min, titrated to 92–96% (88–92% if chronic CO₂ retention), because increasing inspired oxygen corrects impaired gas exchange.
Bronchospasm with wheeze → albuterol 2.5 mg nebulized or 4–8 puffs by MDI with spacer, because β₂-mediated bronchodilation reduces airflow obstruction.
Prominent pleuritic discomfort or fever → acetaminophen 1,000 mg PO/IV every 6 hours as needed, maximum 4 g/day (use ≤3 g/day with liver disease or heavy alcohol use), because it reduces pain and fever.
Suspected pertussis with paroxysmal cough, inspiratory whoop, post-tussive emesis, or a compatible exposure → azithromycin 500 mg PO/IV once, then 250 mg daily on days 2–5, because macrolide therapy reduces transmission; verify local guidance and QT/drug-interaction risk.
Do not give antibiotics for uncomplicated acute bronchitis; they do not meaningfully shorten cough.
Definitive Care & Disposition
Supportive care, hydration, honey for adults, smoking/vaping cessation, and clear return precautions are usually sufficient. Chest radiography is appropriate for fever, tachycardia, tachypnea, hypoxemia, focal crackles, pleuritic pain, frailty, or diagnostic uncertainty. Admit when pneumonia or another serious process produces hypoxemia, sepsis, respiratory failure, or inability to maintain hydration; treat COPD/asthma exacerbation according to that diagnosis.
How This One Kills
Calling colored sputum “bacterial bronchitis” and prescribing antibiotics can delay recognition of pneumonia while exposing the patient to C. difficile infection, allergic reactions, QT prolongation, and resistance.
The Differential — What Else Looks Like This
Pneumonia — fever, tachypnea, hypoxemia, focal crackles, or infiltrate; confusing it with bronchitis delays antibiotics and admission.
Asthma/COPD exacerbation — recurrent obstructive symptoms with diffuse wheeze and reduced airflow; missing it leaves bronchospasm untreated.
Pertussis — prolonged paroxysms, whoop, or post-tussive emesis; missing it permits transmission and complications.
Heart failure — orthopnea, edema, JVP elevation, diffuse crackles; treating as infection delays diuresis and ventilatory support.
The Second-Day Story
Older adults, immunocompromised patients, and those taking antipyretics may have little fever or sputum despite pneumonia. A new functional decline, confusion, unexplained tachypnea, hypoxemia, or focal examination abnormality should override a reassuring cough history; use chest imaging and reassessment rather than the absence of fever as a rule-out test.
Back to Our Patient
Back to the 34-year-old teacher: her normal oxygenation, stable vital signs, lack of focal findings, and cough following a viral prodrome make uncomplicated acute bronchitis most likely. She does not need routine antibiotics or imaging; she receives symptomatic counseling, hydration advice, and return precautions for dyspnea, persistent fever, hypoxemia, or clinical worsening. She is discharged with outpatient follow-up if the cough persists beyond the expected course.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 34-year-old previously healthy teacher with 10 days of cough after an upper-respiratory illness. The cough is now intermittently productive of yellow sputum, but she denies dyspnea, hemoptysis, pleuritic pain, or measured fever. She is afebrile, normocardic, saturating 98% on room air, and has scattered rhonchi that clear with coughing without focal crackles or increased work of breathing. My assessment is uncomplicated acute bronchitis rather than pneumonia, asthma, or heart failure. I plan supportive care without antibiotics, symptomatic treatment as needed, and return precautions for worsening breathing, fever, chest pain, or persistent symptoms.”
Study Directive
Practice distinguishing bronchitis from pneumonia using vital signs and focal examination findings in five mock cases.
Review local chest-radiography indications and antibiotic stewardship guidance.
Write a discharge script that includes expected cough duration and four return precautions.
Reassess one patient with cough after 10 minutes of bronchodilator therapy and document objective response.
Mulhem E, Patalinghug E, Eraqi H · Am Fam Physician, 2025 · PMID 40106287 · cited 1×
A current evidence review for diagnosing uncomplicated acute bronchitis, excluding pneumonia, counseling about expected cough duration, and avoiding antibiotics or other low-value therapies.
More in Today's Issue
3 additional topics
2 of 4
Coronavirus 2019 (COVID-19)
COVID-19 ranges from self-limited illness to rapidly progressive hypoxemic pneumonia, thrombosis, and multiorgan failure. Antivirals benefit selected...
A 67-year-old man arrives with a pulse oximeter clipped to his finger and a damp surgical mask in his hand. He reports four days of fatigue, dry cough, and muscle aches; today, walking from the waiting room left him unusually breathless. At rest he is speaking in full sentences, but his oxygen saturation is 91% on room air and falls to 86% with ambulation. The next decision is whether he can safely leave—or is entering the phase where respiratory decline accelerates.
Before You Read
Which COVID findings mandate escalation rather than outpatient treatment?
Who benefits from antiviral therapy, and how quickly must it start?
When should steroids be used—and when can they harm?
Why It Matters
COVID-19 ranges from self-limited illness to rapidly progressive hypoxemic pneumonia, thrombosis, and multiorgan failure. Antivirals benefit selected high-risk outpatients early, while corticosteroids benefit patients requiring oxygen but may worsen those who are not hypoxemic.
When to Think of It
Fever, cough, sore throat, myalgias, fatigue, anosmia, dyspnea, hypoxemia, or an epidemiologic exposure. Confirm with a high-quality antigen or nucleic-acid test when the result changes isolation or treatment; a negative early antigen test does not fully exclude infection.
Sick or Not Sick
The key call is oxygen requirement and trajectory: stable outpatient disease versus hypoxemic/progressive disease. Measure saturation at rest and with exertion when safe; consider age, immunocompromise, obesity, cardiopulmonary disease, renal/hepatic disease, pregnancy, and vaccination status.
The First Fifteen Minutes
SpO₂ below target or respiratory distress → oxygen by nasal cannula 1–6 L/min, escalating to a nonrebreather at 10–15 L/min if needed, because increased FiO₂ corrects hypoxemia.
High-risk outpatient with mild-to-moderate disease within 5 days of symptom onset → nirmatrelvir/ritonavir 300/100 mg PO twice daily for 5 days if eGFR ≥60; 150/100 mg twice daily if eGFR 30–59; avoid if eGFR <30 unless a specialist/local protocol supports an alternative, because protease inhibition suppresses viral replication. Perform a major drug-interaction and renal review.
High-risk outpatient when Paxlovid is contraindicated, within 7 days → remdesivir 200 mg IV day 1, then 100 mg IV daily days 2–3, because polymerase inhibition limits viral replication; verify renal/hepatic eligibility and local protocol.
Hypoxemic patient requiring supplemental oxygen → dexamethasone 6 mg IV or PO daily, because glucocorticoids suppress dysregulated inflammatory lung injury; do not start routinely in patients who do not require oxygen.
Fever or pain → acetaminophen 1,000 mg PO/IV q6h PRN, maximum 4 g/day, lower with hepatic risk.
Definitive Care & Disposition
Outpatients need isolation guidance, hydration, medication-interaction review, pulse-oximeter instructions when appropriate, and explicit return precautions. Admit for new oxygen requirement, worsening exertional desaturation, respiratory distress, inability to hydrate, altered mental status, or high-risk social circumstances. Escalating oxygen needs may require high-flow nasal oxygen, noninvasive ventilation, or intubation; anticoagulation is based on admission status, bleeding risk, and institutional COVID protocol—not automatically for every outpatient.
How This One Kills
Starting dexamethasone in a nonhypoxemic patient can worsen hyperglycemia, secondary infection, and viral clearance while the actual risk—subclinical or exertional hypoxemia—is missed.
The Atypical Presentation
Older adults may present with weakness, falls, delirium, anorexia, or worsening chronic disease rather than fever and cough. Vaccination or partial treatment may blunt symptoms while hypoxemia persists; trend exertional saturation, respiratory rate, work of breathing, and function rather than relying on fever or auscultation alone.
Back to Our Patient
Back to the 67-year-old man: his exertional desaturation and resting saturation of 91% identify hypoxemic COVID rather than uncomplicated outpatient infection. He receives supplemental oxygen, confirmatory testing and evaluation for pneumonia, and dexamethasone because he requires oxygen; antiviral selection depends on symptom timing, renal function, and drug interactions. Because he has a new oxygen requirement and worsening exertional symptoms, he is admitted for monitored respiratory support and reassessment for thrombotic or bacterial complications.
Patient Presentation to Attending
“This is a 67-year-old man with four days of fatigue, myalgias, and dry cough who developed exertional dyspnea today. He has no chest pain, hemoptysis, syncope, or leg swelling, but his oxygen saturation is 91% at rest and falls to 86% with ambulation. He is mildly tachypneic, speaking full sentences, and has bilateral fine crackles without shock or altered mental status. COVID testing is pending, and I will obtain chest imaging and basic labs while starting supplemental oxygen. My leading diagnosis is hypoxemic COVID pneumonia; I plan dexamethasone, evaluation for PE or bacterial coinfection if clinically indicated, and hospital admission.”
Study Directive
Memorize outpatient antiviral windows, renal dose adjustments, and the major contraindicated medication classes.
Work through three cases deciding outpatient care versus admission using resting and exertional oxygenation.
Review your institution’s anticoagulation and oxygen-escalation pathways.
Practice a 60-second medication-interaction screen for a patient taking anticoagulants, antiarrhythmics, statins, and anticonvulsants.
Key Medications
Nirmatrelvir/ritonavir: 300/100 mg PO BID ×5 days if eGFR ≥60; 150/100 mg BID if eGFR 30–59; dosing/eligibility and interactions require Lexicomp, UpToDate, or institutional protocol.
Remdesivir: 200 mg IV day 1, then 100 mg IV daily days 2–3 for outpatient early therapy; inpatient duration varies by severity and protocol.
Dexamethasone: 6 mg IV/PO daily for patients requiring oxygen; duration commonly up to 10 days or until discharge, per protocol.
Enoxaparin prophylaxis for admitted patients when indicated: commonly 40 mg SC daily; adjust for renal dysfunction, obesity, and institutional COVID guidance.
Pediatric dosing differs substantially; use an age/weight-based pediatric protocol.
High-Yield Pearls
A normal resting saturation does not exclude clinically important exertional hypoxemia.
Paxlovid is a medication-reconciliation problem: ritonavir interactions can be more dangerous than COVID itself.
COVID does not eliminate the usual differential for dyspnea, especially PE, ACS, and heart failure.
The Mimics
Influenza — abrupt fever, prominent myalgias, and positive influenza testing; confusing them may miss time-sensitive antiviral treatment.
Pulmonary embolism — disproportionate tachycardia, pleuritic pain, syncope, or hypoxemia; attributing all dyspnea to COVID delays anticoagulation and reperfusion decisions.
Bacterial pneumonia — focal consolidation, lobar infiltrate, or shock; missing it delays antibiotics and source evaluation.
A 72-year-old woman with confirmed COVID-19 has SpO₂ 88% on room air and requires 3 L/min oxygen. Which therapy has the strongest evidence for reducing mortality from the inflammatory pulmonary phase?
ADexamethasone
BRoutine azithromycin
CIvermectin
DDexamethasone only if she develops fever
Reveal answer
Correct: A
Systemic corticosteroids benefit patients requiring supplemental oxygen. They are not routinely indicated for mild COVID without hypoxemia.
3 of 4
Fat Embolism Syndrome
Fat embolism syndrome is an uncommon but potentially fatal complication of long-bone or pelvic trauma, usually developing after a latent interval. Diagnosis...
0:00 / –:––AI‑generated audio
The Case
A 23-year-old man with a femur fracture lies restless beneath a warm blanket, his face flushed and speckled with tiny red-purple dots across the upper chest. Hours earlier he was alert after the crash; now he is confused and breathing rapidly, with an oxygen saturation of 89% despite a nasal cannula. His chest radiograph shows new bilateral hazy opacities, but there is no single laboratory result waiting to name the problem. The team must decide whether this is evolving post-traumatic respiratory failure—and how aggressively to support him.
Before You Read
What clinical triad should trigger concern for fat embolism syndrome?
How do you distinguish it from pulmonary thromboembolism, aspiration, and pulmonary contusion?
What immediate intervention changes the patient’s trajectory?
Why It Matters
Fat embolism syndrome is an uncommon but potentially fatal complication of long-bone or pelvic trauma, usually developing after a latent interval. Diagnosis is clinical; waiting for a confirmatory test delays oxygenation, fracture stabilization, and treatment of competing life threats.
When to Think of It
Typically 12–72 hours after femur, tibia, or pelvic fracture or intramedullary manipulation: hypoxemia, respiratory distress, neurologic changes, and petechial rash. Fever, tachycardia, thrombocytopenia, anemia, and diffuse infiltrates support but do not establish the diagnosis.
Sick or Not Sick
The key call is respiratory or neurologic instability requiring ICU-level support. Assess airway protection, oxygenation, ventilation, mental status, hemodynamics, associated trauma, and alternate causes such as PE, aspiration, sepsis, and head injury.
The First Fifteen Minutes
SpO₂ below target → oxygen by nasal cannula 1–6 L/min, escalating to a nonrebreather at 10–15 L/min, because hypoxemia is the immediate physiologic threat.
Persistent hypoxemia or increased work of breathing → high-flow nasal oxygen, commonly starting 40–60 L/min and titrating FiO₂, because it provides reliable oxygen delivery and modest airway pressure.
Failure to protect the airway, severe fatigue, or refractory hypoxemia → RSI with etomidate 0.3 mg/kg IV and rocuronium 1.2 mg/kg IV, because controlled ventilation and airway protection are required; use local trauma-airway protocol and adjust for physiology.
Shock after trauma → balanced crystalloid 500–1,000 mL IV bolus with reassessment, because cautious volume restoration supports perfusion while avoiding worsening lung edema; activate blood-product resuscitation when hemorrhage is suspected.
Do not routinely give corticosteroids, heparin, aspirin, or albumin specifically for FES; none is established rescue therapy.
Definitive Care & Disposition
Admit to the ICU for serial oxygenation, neurologic checks, blood gases as needed, and evaluation for associated injuries. Obtain chest imaging, CBC, metabolic studies, ECG, and targeted testing; CT pulmonary angiography is reserved for meaningful PE concern and should not delay stabilization. Early orthopedic consultation and definitive fracture stabilization are central; use lung-protective ventilation if intubated, with tidal volume about 6–8 mL/kg predicted body weight and PEEP titrated to oxygenation/hemodynamics. There is no validated single diagnostic test or universally accepted medication cure.
How This One Kills
Attributing the deterioration to “just trauma” or waiting for a positive fat-globule test allows progressive hypoxemic respiratory failure and cerebral fat embolism to advance; fat-laden macrophage inflammation, not merely mechanical embolic obstruction, drives the syndrome.
The Atypical Presentation
The petechial rash may be absent, transient, or hidden under dressings, and hypoxemia may be masked by supplemental oxygen. A patient who becomes newly confused, tachypneic, thrombocytopenic, or increasingly oxygen-dependent 1–3 days after long-bone trauma should prompt a syndrome-level diagnosis even when CT angiography is nondiagnostic and there is no dramatic rash.
Back to Our Patient
Back to the 23-year-old man: the delayed onset after femur fracture, new hypoxemia, tachypnea, confusion, petechiae, and bilateral infiltrates strongly suggest fat embolism syndrome after immediate exclusion of hemorrhage, tension pneumothorax, head injury, aspiration, and PE. He receives escalating oxygen and is transferred to the ICU; because his oxygenation and mental status worsen, the airway is secured with RSI and lung-protective ventilation. Orthopedics urgently stabilizes the fracture, and he remains admitted for supportive critical care rather than receiving empiric anticoagulation or steroids for FES alone.
Patient Presentation to Attending
“This is a 23-year-old man with a femur fracture from a motor-vehicle collision who, approximately 24 hours later, developed acute confusion, tachypnea, and worsening hypoxemia. He has a new petechial rash over the upper chest, bilateral hazy infiltrates, and an oxygen saturation of 89% despite nasal cannula; there is no reported emesis, unilateral leg swelling, or focal neurologic deficit. I am concerned for fat embolism syndrome, while continuing to evaluate for PE, aspiration, pulmonary contusion, and occult head injury. I will escalate oxygen, assess airway protection and hemodynamics, obtain trauma-directed labs and imaging, and involve ICU and orthopedics urgently. If he cannot maintain oxygenation or mental status, I recommend RSI and lung-protective ventilation.”
Study Directive
Draw the three-part FES syndrome—respiratory, neurologic, petechial—in 30 seconds from memory.
Compare FES, PE, aspiration, and pulmonary contusion in four trauma vignettes.
Review your trauma airway and lung-protective ventilation protocols.
Practice stating why anticoagulation and steroids are not routine FES therapy.
Key Medications
Oxygen and ventilatory support are primary therapy; no medication reverses FES.
Etomidate for RSI: 0.3 mg/kg IV; consider lower dosing in frail or profoundly unstable patients.
Rocuronium for RSI: 1.2 mg/kg IV.
Balanced crystalloid: 500–1,000 mL IV bolus with frequent reassessment; trauma hemorrhage may require blood products instead.
Analgesia when needed: fentanyl 25–50 mcg IV titrated every 5 minutes; use caution with respiratory depression and hypotension.
Steroids for prophylaxis or treatment are not routinely recommended; check trauma/critical-care protocol if considering an unusual case.
High-Yield Pearls
The classic latent interval of 12–72 hours after long-bone trauma is a powerful discriminator.
A negative fat-globule test does not exclude FES; the test is neither sensitive nor specific enough to guide care.
Cerebral FES may occur without severe pulmonary findings, presenting as unexplained encephalopathy after orthopedic trauma.
The Mimics
Pulmonary thromboembolism — pleuritic pain, RV strain, or focal vascular findings; confusing it with FES may lead to unnecessary anticoagulation while missing fracture stabilization.
Pulmonary contusion — infiltrate immediately adjacent to chest trauma, often present early; delayed diffuse deterioration favors FES.
Aspiration pneumonitis — witnessed emesis or depressed consciousness with dependent infiltrates; missing it can lead to inappropriate assumptions about the source of hypoxemia.
Diffuse axonal injury — severe neurologic dysfunction with traumatic brain injury findings; attributing coma to FES can miss urgent neurosurgical management.
Board Question
A 26-year-old with a femoral shaft fracture develops hypoxemia, confusion, fever, thrombocytopenia, and a petechial rash 36 hours later. Chest imaging shows bilateral diffuse opacities. What is the most appropriate treatment?
AImmediate systemic anticoagulation
BHigh-dose corticosteroids
CSupportive respiratory care and early fracture stabilization
Fat embolism syndrome is a clinical diagnosis treated primarily with oxygenation, ventilatory support, ICU care, and fracture stabilization. Routine anticoagulation and corticosteroids are not established treatments.
A current trauma-focused reference on recognizing the respiratory, neurologic, and petechial manifestations of fat embolism syndrome and initiating supportive emergency management.
Identifies the incidence and risk factors for fat embolism after isolated lower-extremity long-bone fractures, helping clinicians target surveillance toward higher-risk trauma patients.
4 of 4
PREOXI Study
Peri-intubation hypoxemia is common and can rapidly cause dysrhythmia, cardiac arrest, and neurologic injury. PREOXI provides randomized evidence that...
A 58-year-old woman with septic shock lies pale and sweaty on the resuscitation bed, her voice interrupted by rapid breaths. Her oxygen saturation is 94% on a nonrebreather, but she is tiring, hypotensive, and likely to need a definitive airway. The laryngoscope, suction, and ventilator are ready; the unresolved question is how to buy the safest oxygen reserve before the first attempt.
Before You Read
Which preoxygenation strategy best prevents peri-intubation hypoxemia?
When should noninvasive ventilation be preferred over high-flow nasal oxygen?
What must happen in parallel with preoxygenation?
Why It Matters
Peri-intubation hypoxemia is common and can rapidly cause dysrhythmia, cardiac arrest, and neurologic injury. PREOXI provides randomized evidence that noninvasive ventilation can reduce hypoxemia compared with high-flow nasal oxygen during preoxygenation in critically ill adults.
When to Think of It
Any critically ill patient likely to require intubation—especially those with acute hypoxemic respiratory failure, obesity, shunt physiology, pulmonary edema, or low functional residual capacity—needs a deliberate preoxygenation plan rather than simply placing a standard nasal cannula.
Sick or Not Sick
The key call is whether the patient can tolerate noninvasive ventilation and whether immediate airway control is required. Severe agitation, vomiting, inability to protect the airway, facial trauma, or immediate arrest physiology may make NIV unsafe or delay intubation; prepare for rapid failure in all high-risk patients.
The First Fifteen Minutes
Patient breathing spontaneously and able to protect the airway, particularly with hypoxemic respiratory failure → NIV with tight mask, commonly inspiratory pressure 10–15 cm H₂O and expiratory pressure 5–8 cm H₂O, FiO₂ 1.0 for approximately 3 minutes, because positive pressure recruits alveoli and increases oxygen reservoir; adjust to synchrony and local protocol.
NIV contraindicated or poorly tolerated, or less severe oxygenation deficit → HFNC at 40–60 L/min with FiO₂ 1.0, because high flow provides high inspired oxygen and some apneic oxygenation.
Persistent desaturation during preparation → add nasal cannula at 15 L/min beneath the NIV or mask when feasible, because oxygen delivery may continue during laryngoscopy; this is an adjunct, not a substitute for effective preoxygenation.
Hypotension before induction → balanced crystalloid 250–500 mL IV if fluid responsive and not overloaded, because preload optimization can reduce peri-induction collapse; initiate vasopressor support when needed.
Shock with persistent MAP below 65 mm Hg despite appropriate fluid assessment → norepinephrine 0.05–0.1 mcg/kg/min IV infusion, titrated to MAP ≥65, because α-mediated vasoconstriction preserves perfusion during induction; use institutional concentration and infusion protocol.
When intubation is unavoidable → ketamine 1–2 mg/kg IV or etomidate 0.3 mg/kg IV for induction, followed immediately by rocuronium 1.2 mg/kg IV, because paralysis improves first-pass conditions and controlled airway access; select induction agent based on hemodynamics and local protocol.
Definitive Care & Disposition
PREOXI was a multicenter randomized trial of critically ill adults undergoing tracheal intubation, comparing NIV with HFNC for preoxygenation. NIV reduced hypoxemia during intubation compared with HFNC—approximately 13% versus 27% in the published primary analysis—without eliminating the need for positioning, suction, hemodynamic preparation, and rescue oxygenation. After intubation, confirm tube placement with continuous waveform capnography, secure the tube, initiate lung-protective ventilation, and treat the underlying disease. ICU disposition is expected for patients requiring invasive ventilation or vasopressors.
How This One Kills
Treating preoxygenation as an oxygen-device choice while ignoring hypotension, delayed preparation, or poor mask seal allows a patient to arrest during induction; even the best device cannot compensate for inadequate time, positioning, or hemodynamic planning.
The Atypical Presentation
A patient may appear comfortable with a saturation of 100% while receiving high-flow oxygen yet desaturate within seconds after induction because the apparent reserve is low. Obesity, pregnancy, severe shunt, pulmonary edema, and metabolic acidosis shorten safe apnea time; use physiology and trajectory—not the monitor number alone—to choose NIV, maximize preparation, and position head-up.
Back to Our Patient
Back to the 58-year-old woman: she is critically ill, tiring, and hypotensive but still protecting her airway, so the team places her head-up, seals NIV at 100% oxygen, and preoxygenates while suction, video laryngoscopy, backup devices, and vasopressor support are prepared. Her blood pressure remains low, prompting norepinephrine before induction; after adequate preparation she receives a hemodynamically appropriate induction agent and rocuronium, followed by first-pass intubation and waveform capnography confirmation. She is admitted to the ICU for mechanical ventilation and septic-shock management.
Patient Presentation to Attending
“This is a 58-year-old woman with septic shock and worsening respiratory fatigue who requires intubation. She is tachypneic, diaphoretic, and hypotensive, with an SpO₂ of 94% on a nonrebreather, but she is still protecting her airway and has no active emesis or facial trauma. I recommend head-up NIV preoxygenation at FiO₂ 1.0 while we prepare suction, video laryngoscopy, backup oxygenation, and norepinephrine for peri-induction support. Because she is at high risk for hypoxemia and cardiovascular collapse, I will optimize her blood pressure, then perform RSI with a hemodynamically appropriate induction agent and rocuronium. After intubation I will confirm placement with waveform capnography, begin lung-protective ventilation, and admit her to the ICU.”
Study Directive
Rehearse a 90-second pre-intubation checklist including position, device, seal, suction, backup airway, vasopressor, and post-intubation plan.
Memorize the PREOXI comparison and primary clinical outcome without overgeneralizing it to patients excluded from the trial.
Practice selecting NIV versus HFNC in five cases involving vomiting, agitation, pulmonary edema, severe asthma, and facial trauma.
Review your institution’s RSI medication concentrations and vasopressor infusion setup.
Key Medications
Norepinephrine: start 0.05–0.1 mcg/kg/min IV infusion, titrate to MAP ≥65; concentration varies—follow institutional protocol.
Ketamine: 1–2 mg/kg IV for induction; consider lower dosing in profound shock.
Etomidate: 0.3 mg/kg IV for induction; dosing may be reduced in frail or severely unstable patients.
Rocuronium: 1.2 mg/kg IV for RSI.
Phenylephrine, if transient vasodilation is the dominant problem and heart rate is adequate: 50–200 mcg IV boluses, or infusion per protocol; verify local dosing guidance.
Pediatric preoxygenation and RSI doses are weight-based and differ; use a pediatric airway protocol.
High-Yield Pearls
NIV is particularly valuable when low FRC or shunt physiology makes conventional preoxygenation unreliable.
Preoxygenation and cardiovascular preparation must occur simultaneously; peri-intubation arrest is often hemodynamic, not purely respiratory.
HFNC remains useful when NIV is contraindicated or intolerable and for continued oxygen delivery during laryngoscopy.
The Mimics
Apneic oxygenation — nasal oxygen alone during laryngoscopy; it may prolong safe apnea but does not replace alveolar denitrogenation with effective preoxygenation.
Bag-mask ventilation — positive-pressure rescue or bridge; excessive ventilation before paralysis can insufflate the stomach and increase aspiration risk.
Delayed-sequence intubation — medication-facilitated preoxygenation in an agitated patient; confusing it with routine RSI may leave the patient inadequately oxygenated.
Awake intubation — spontaneous ventilation preserved with topicalization; choosing routine RSI in an anticipated difficult airway risks catastrophic loss of the airway.
Board Question
In the PREOXI randomized trial, which preoxygenation strategy was associated with less hypoxemia during intubation of critically ill adults?
AStandard nasal cannula at 2 L/min
BNoninvasive ventilation
CNo preoxygenation followed by immediate RSI
DBag-mask ventilation with zero PEEP
Reveal answer
Correct: B
PREOXI found less hypoxemia with NIV than with HFNC during preoxygenation in critically ill adults. The strategy still requires careful patient selection, positioning, hemodynamic preparation, and rescue planning.
Synthesizes randomized evidence across preoxygenation methods, helping clinicians compare noninvasive ventilation with oxygen mask and other strategies for preventing peri-intubation hypoxemia.
The PREOXI trial showed that noninvasive ventilation used for preoxygenation reduced hypoxemia during emergency intubation of critically ill adults compared with an oxygen mask.
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 62-year-old woman presents with a few hours of palpitations and mild breathlessness. She is comfortable, with a blood pressure of 128/76 and a regular pulse around 120. What’s the diagnosis, and the first move?
Check your answer
Focal Atrial Tachycardia. Distinguish focal AT from flutter and MAT because treatment diverges, and hunt for a precipitant. If the P-wave and rate picture suggests digoxin toxicity, check the level and reconsider AV nodal agents rather than pushing more.
From the July 26 edition
Today, three days ago: Propofol. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
Procedural sedation: 0.5–1 mg/kg IV, then 0.25–0.5 mg/kg increments. Post-intubation sedation: commonly 5–50 mcg/kg/min infusion titrated to sedation/BP. Hemodynamic instability/shock relative, egg/soy allergy no longer absolute in many policies but check local guidance, hypersensitivity.
From the July 19 edition
A 24-year-old athlete with known HOCM develops hypotension and tachycardia after several hours of vomiting. He has a hyperdynamic LV and systolic anterior motion of the mitral valve. Which intervention is most appropriate?
ADobutamine infusion
BNitroglycerin infusion
CPhenylephrine infusion
DFurosemide 80 mg IV
Reveal answer
Correct · C
Phenylephrine infusion. Pure α-mediated vasoconstriction increases afterload and reduces the dynamic LVOT gradient without increasing contractility. Dobutamine, nitroglycerin, and aggressive diuresis may worsen obstruction.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Dr. Tannenbaum returns with a case of prolonged QT and a dangerous arrhythmia. The post ECG Pointers: Long Intervals and Squiggly Lines appeared first on emDocs .
In this episode, Sam Ashoo, MD and Dr. T.R. Eckler, MD discuss the June 2026 Emergency Medicine Practice article, Diagnosis and Management of Heat Stroke and Other Heat-Related Illness in the Emergency Department 0:21 Intro & Promo 0:56 Episode Introduction 3:14 Spectrum of Heat-Related Illnesses 7:37 Differential Diagnosis 8:58 Pre-Hospital Management...
The YEARS protocol has gained popularity as a straightforward approach to identify a subset of patients undergoing a workup for suspected pulmonary embolism (PE) who are at sufficiently low risk to safely use a...
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
Fat embolism syndrome links post-traumatic hypoxaemia, neurological change, and petechiae to a largely supportive critical-care strategy focused on oxygenation and ventilation.
A syndrome caused by systemic embolisation of fat globules released into the circulation following trauma or surgical procedures
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Vancomycin (oral)
Glycopeptide (oral, non-absorbed)
Indication
Clostridioides difficile infection, including severe and fulminant disease. Not absorbed systemically — no role in systemic infection.
What’s your dose? — reveal dosing & cautions
ED Dose
125 mg PO QID x10 days (non-severe and severe CDI). Fulminant: 500 mg PO/NG QID, plus IV metronidazole; add rectal vancomycin retention enema (500 mg in 100 mL saline q6h) if ileus is present.
Renal Adjustment
None — negligible systemic absorption.
Contraindications
Hypersensitivity to vancomycin.
Interactions
Negligible systemic interactions.
Monitoring
Clinical response; consider serum levels only in fulminant colitis with prolonged high-dose therapy or significant renal impairment.
ED Pearl
Oral and IV vancomycin are not interchangeable: IV vancomycin does NOT treat C. difficile (it doesn't reach the gut lumen), and oral vancomycin does NOT treat systemic infection. For fulminant CDI with ileus, add a rectal vancomycin enema.
ED Pearl
Nicardipine is for controlled descent, not BP free-fall — set a disease-specific target and titrate, especially in brain bleeds and ischemic stroke.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Toxicology
Digoxin Effect
Sagging 'reverse-tick' ST depression with a short QT means the patient takes digoxin — it does not mean they are toxic.
The Tracing
A 70-year-old woman on long-standing digoxin for atrial fibrillation comes in for a pre-operative evaluation, entirely asymptomatic. Her ECG catches your eye: across the lateral leads V4-6, I and aVL, the ST segments sag downward in a smooth downsloping curve that looks like a reverse tick — a shape someone once dubbed Salvador Dali's moustache. The T waves are biphasic, dipping negative first and then rising to a small terminal peak continuous with the depressed ST segment. The QT interval looks short, the PR is mildly long, and there are prominent U waves. You find yourself wondering whether this tracing is telling you she is poisoned.
Downsloping ('sagging') ST depression with the characteristic reverse-tick / Salvador Dali moustache morphology
Shortened QT interval
Biphasic T waves (initial negative, terminal positive deflection), typically in leads with a dominant R wave such as V4-6
Mild PR prolongation (up to ~240 ms from increased vagal tone), prominent U waves, and J-point depression in leads with tall R waves
Pearls
Digoxin effect is a therapeutic-dose phenomenon: it tells you the patient is on digoxin, not that they are toxic — the two are distinct entities.
The short QT and sagging morphology, with the T wave continuous with the depressed ST segment, are the fingerprints that separate it from primary ischemia.
The mechanism is intuitive: shortened refractory periods give the short QT and repolarization changes, while increased vagal tone at the AV node lengthens the PR.
Pitfalls
Mistaking the J-point depression and sagging ST for left ventricular hypertrophy — the short QT, inferior sagging, and absent LVH voltage criteria give it away.
Reading the ST depression as active ischemia and launching an ACS workup in an asymptomatic patient with classic digoxin effect.
Conversely, dismissing the whole tracing as 'just digoxin effect' and missing signs of true toxicity — frequent PVCs or other ectopy on the same ECG should raise that concern.
At the Bedside
Recognize digoxin effect as an expected finding rather than an emergency: do not treat it as ischemia or LVH, but do scrutinize the same tracing for ectopy or arrhythmia that would signal genuine digoxin toxicity and change management.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · Bronchitis
Self-Examination
Test Your Understanding
A 29-year-old healthy adult has 8 days of cough after rhinorrhea. Temperature is 37.2°C, respiratory rate 16/min, oxygen saturation 99%, and lung examination reveals diffuse rhonchi that clear with cough. Sputum is yellow. What is the best management?
AAmoxicillin-clavulanate
BAzithromycin
CChest radiograph and supportive care
DSupportive care without routine antibiotics
Reveal answer
Correct answer · D
Acute bronchitis is generally viral; sputum color does not distinguish bacterial infection. Imaging is unnecessary when pneumonia is unlikely based on stable vitals and examination.
Study Pace4 topics today; Issue 15 of 94 — Pulmonary (Week 9 A)Deadline · June 1, 2026