An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Infections of the Spinal Column
Missed spinal infection can progress from back pain to irreversible paralysis, spinal instability, bacteremia, and death. The key is to recognize when “back pain” is actually a source-control problem with neurologic stakes.
A 58-year-old man sits rigidly on the stretcher, one hand pressed to the base of his neck, the other worrying at the sheets as the monitor soft-pings in the background. He smells faintly of sweat and stale clothes; the T-shirt under his sweatshirt is damp despite the cool room. He says the pain has been “deep” for days, now worse when he coughs, and this morning his right leg felt “like it wasn’t mine” climbing stairs. He has a low-grade fever, a murky story of back pain, and a bladder that suddenly feels unreliable — but no one has named the problem yet.
— What’s your move? Read on.
Before you read
Which findings mean the cord or cauda equina may already be threatened?
What do you start before imaging if the patient is septic or neurologically worsening?
When to Think of It
Think spinal column infection when severe focal back or neck pain is paired with fever, elevated inflammatory markers, bacteremia, IV drug use, recent spinal procedure, immunosuppression, dialysis, diabetes, or new neurologic symptoms. Night pain, pain with percussion, radicular pain, gait change, saddle anesthesia, urinary retention, or unexplained weakness should push this high on the list.
Sick or Not Sick
The fork is neurologically intact and hemodynamically stable vs. spinal cord/cauda equina compromise or sepsis. Any objective weakness, urinary retention, saddle anesthesia, progressive sensory loss, hypotension, or altered mental status means emergent action and likely surgical involvement now.
The First Fifteen Minutes
Sepsis/hypotension → 30 mL/kg balanced crystalloid IV; if MAP remains low after fluids, norepinephrine infusion 0.05–1 mcg/kg/min IV because perfusion buys time for source control.
High suspicion with fever, bacteremia, or systemic toxicity → obtain blood cultures x2 before antibiotics if this does not delay treatment, then start empiric antibiotics immediately:
Vancomycin 15–20 mg/kg IV q8–12h plus cefepime 2 g IV q8h if concern for epidural abscess/hematogenous spread or healthcare exposure, because you need MRSA and gram-negative coverage early.
If severe beta-lactam allergy: vancomycin 15–20 mg/kg IV plus aztreonam 2 g IV q8h; local protocols vary, so check an antibiogram/reference.
If contiguous source or vertebral osteomyelitis/discitis with anaerobic risk: broaden per local protocol; many centers use vancomycin + ceftriaxone 2 g IV daily or vancomycin + piperacillin-tazobactam 4.5 g IV q6h when polymicrobial infection is plausible.
Neurologic deficit or cauda equina features → urgent MRI with contrast of the involved spine region; if MRI delayed/unavailable and suspicion is high, escalate immediately because time equals neural tissue.
Severe pain → hydromorphone 0.5–1 mg IV q2–3h PRN or fentanyl 25–50 mcg IV q10–15 min PRN; analgesia helps exam and imaging tolerance.
Bladder symptoms → bedside bladder scan; if retention, place Foley because it clarifies neuro compromise and protects the kidneys.
Definitive Care & Disposition
MRI defines extent, abscess burden, osteomyelitis/discitis, and cord compression. Neurosurgery/orthopedic spine and infectious diseases should be involved early when there is an abscess, instability, neurologic deficit, or bacteremia; drainage or decompression may be urgent. Most patients need admission, often stepdown/ICU if septic or neurologically impaired. Tailor antibiotics to cultures; duration is typically prolonged and depends on organism, hardware, abscess, and source control.
How This One Kills
The classic failure is dismissing focal back pain as musculoskeletal until the patient develops an irreversible motor deficit or urinary retention. Another dangerous miss is delaying antibiotics and spine consultation while waiting for “perfect” imaging logistics.
The Differential — What Else Looks Like This
Mechanical back strain — pain is positional and lacks fever, bacteremia, or neurologic change; confusing it delays MRI and antibiotics.
Spinal fracture — clear trauma/osteoporosis/steroid history and focal bony tenderness; missing it risks instability or cord injury.
Cauda equina syndrome from disc herniation — similar bladder and saddle symptoms, but no infectious clues; confusing the two delays source control or surgery.
Metastatic spinal disease — constitutional symptoms and night pain may overlap, but a cancer history and noninfectious imaging pattern steer management away from antibiotics.
The Second-Day Story
Older adults, immunocompromised patients, and people pretreated with antibiotics may have little or no fever and only vague malaise, falls, or worsening chronic back pain. ESR/CRP may be the first real clue, and bacteremia may be the only microbiologic hint. In the diabetic or dialysis patient with new back pain plus gait change, treat the story as infectious until proven otherwise, even if the skin exam is bland and the neuro exam is still “mostly okay.”
Back to Our Patient
Back to our 58-year-old with deep neck/back pain, fever, and new right-leg heaviness: this is Infections of the Spinal Column until proven otherwise. He is at risk for spinal cord compromise because his neuro symptoms are new and evolving, so the move is cultures, immediate broad-spectrum IV antibiotics, urgent MRI of the symptomatic spine, bladder scan, and emergent spine consultation. If MRI shows an epidural collection or compression, he needs source control and likely decompression, with admission at least to a monitored bed and ICU if septic or worsening.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“58-year-old man with diabetes and IVDU history presenting with 4 days of severe focal neck/back pain and new right-leg weakness, plus fever to 38.3 and urinary hesitancy. He has pain with percussion over the cervical/thoracic spine, elevated ESR/CRP, and a bladder scan showing retention; no trauma and no isolated radicular pain to suggest simple strain. Exam shows mild unilateral leg drift and no cranial findings; he is hemodynamically stable right now. I’m concerned for spinal infection with possible epidural abscess/vertebral osteomyelitis causing early cord compromise. I’ve drawn blood cultures and started vancomycin plus cefepime, and I want urgent MRI with spine consult and admission.”
Study Directive
Draw the pathway from focal spinal pain → bacteremia/ESR/CRP → MRI → antibiotics/source control from memory.
Make a one-page comparison of epidural abscess vs. vertebral osteomyelitis/discitis vs. cauda equina.
Practice an ED order set: blood cultures, CBC/CMP/ESR/CRP, MRI with contrast, empiric antibiotics, bladder scan, spine consult.
Teach-back drill: present a 1-minute case where the only clue is “back pain plus trouble walking.”
Review local empiric antibiotic choices for MRSA + gram-negative spinal infection coverage.
Tande AJ, Currier BL, Osmon DR · N Engl J Med, 2026 · PMID 42019020 · cited 1×
A high-yield reference for recognizing spinal epidural abscess early—think severe back pain plus fever, neurologic deficit, or risk factors—and moving quickly to MRI, antibiotics, and spine/neurosurgical consultation.
More in Today's Issue
3 additional topics
2 of 4
Transverse Myelitis
Inflammatory myelitis can cause rapid paraplegia, autonomic dysfunction, and permanent disability if treatment is delayed. It also overlaps with compressive...
A 34-year-old woman in a wool coat keeps tugging at her sleeves because the exam room feels “like ice water,” though she’s warm to the touch. She says that yesterday her feet were buzzing, and by this morning she was tripping on the curb and couldn’t quite trust her bladder. The neuro exam is messy in a way that makes people rush past it: strength fading, reflexes changing, a sensory line on her torso. The spine MRI is being arranged, but the real question is what the pattern means before the image lands.
Before You Read
What makes a spinal cord syndrome inflammatory rather than compressive?
Which exam pattern separates myelopathy from peripheral neuropathy?
What is the ED move when transverse myelitis is on the table?
Why It Matters
Inflammatory myelitis can cause rapid paraplegia, autonomic dysfunction, and permanent disability if treatment is delayed. It also overlaps with compressive and infectious spinal emergencies, so missing the pattern is a major ED error.
When to Think of It
Think transverse myelitis in a patient with acute/subacute bilateral weakness, sensory level, and bladder/bowel dysfunction not explained by trauma or compression. Painful back symptoms can occur, but the clue is a spinal cord syndrome: upper motor neuron signs below the lesion, band-like truncal sensory change, and sometimes asymmetric onset that becomes bilateral.
Sick or Not Sick
The fork is cord compression/infection/vascular lesion vs. isolated inflammatory myelitis. Any severe back pain, fever, cancer history, trauma, anticoagulation, or rapidly progressive deficit means you must exclude compressive causes first with urgent MRI.
The First Fifteen Minutes
Suspected compressive lesion cannot be excluded → urgent MRI entire symptomatic spine with and without contrast and spine/neurosurgery consultation; do not anchor on “myelitis” before ruling out a surgical lesion.
High likelihood inflammatory myelitis after compression is excluded → methylprednisolone 1 g IV daily for 3–5 days, because high-dose steroids reduce inflammatory injury and may improve recovery.
Significant weakness, respiratory compromise, or autonomic instability → admit; consider ICU if ventilatory/pressor support is a concern because respiratory muscles and autonomic pathways can deteriorate.
If infectious myelitis/epidural abscess remains possible → blood cultures and empiric antibiotics before steroids or alongside them if unstable, because immunosuppression can worsen untreated infection.
Urinary retention → Foley catheter because bladder decompression improves comfort and tracks neurologic severity.
Definitive Care & Disposition
Diagnosis is usually MRI plus CSF after compression is excluded; LP can show pleocytosis and elevated protein, and serologies may reveal MS, NMOSD, MOG-associated disease, or postinfectious causes. Neurology should guide steroid taper, plasma exchange for steroid-refractory cases, and longer-term disease-specific therapy. Admit all patients with significant deficits; discharge is uncommon from the ED.
How This One Kills
The fatal error is giving “just steroids” to a patient whose cord is actually compressed or infected. The opposite miss is waiting on LP or outpatient workup while weakness and bladder dysfunction are evolving.
The Atypical Presentation
Elderly patients may present with falls, gait decline, or urinary retention before they can describe a sensory level. Partial treatment, prior steroids, or concurrent infection can blunt the exam and blur the timeline. If the exam suggests a cord process but the story is muddy, keep compressive and inflammatory causes both alive until MRI settles it.
Back to Our Patient
Back to our 34-year-old with bilateral leg tingling, a torso sensory line, and bladder trouble: the pattern is a spinal cord syndrome, so transverse myelitis is a major consideration only after compression is excluded. She needs urgent MRI of the symptomatic spine to rule out abscess or mass, Foley if retention is present, and neurology involvement. If imaging excludes compression and the syndrome fits inflammatory myelitis, start IV methylprednisolone and admit for ongoing neurologic monitoring and etiologic workup.
Patient Presentation to Attending
“34-year-old woman with 2 days of progressive bilateral leg numbness and weakness, urinary urgency turning into retention, and a clear sensory level around the mid-abdomen. She has no trauma, no fever, and no back tenderness, but exam shows asymmetric leg weakness, hyperreflexia below the lesion, and decreased pinprick below the torso line. I’m worried about an acute myelopathy; epidural abscess and compression still need urgent MRI exclusion. If MRI is negative for compression, I’d treat presumptive transverse myelitis with IV steroids and admit with neurology.”
Practice distinguishing transverse myelitis vs. epidural abscess vs. GBS from a 30-second vignette.
Write the ED sequence: MRI first if compression possible → steroids if inflammatory → admit.
Review when to escalate to plasma exchange for steroid-refractory disease with neurology.
Memorize one common association set: MS, NMOSD, MOGAD, postinfectious.
Key Medications
Methylprednisolone 1 g IV daily for 3–5 days.
Hydromorphone 0.5–1 mg IV q2–3h PRN or fentanyl 25–50 mcg IV q10–15 min PRN for pain.
Lorazepam 0.5–2 mg IV PRN if severe anxiety/spasm is interfering with care, used sparingly. Pediatric steroid dosing and escalation to plasma exchange are protocol-dependent; check a reference.
High-Yield Pearls
A sensory level is a spinal cord clue, not a peripheral neuropathy clue.
Always ask: could this be compression? If yes, MRI first — steroids second.
Bladder dysfunction in myelopathy is a severity marker, not a benign associated symptom.
The Mimics
Spinal epidural abscess — fever, back pain, and neurologic deficit with bacteremia risk; confusing it with myelitis delays drainage and antibiotics.
Multiple sclerosis relapse — often prior episodes and multifocal CNS signs; missing alternative inflammatory etiologies can change long-term therapy.
Spinal cord infarction — abrupt onset and vascular risk factors; confusing it with myelitis may delay vascular evaluation.
Guillain-Barre syndrome — areflexia and ascending weakness with no sensory level; confusing it with myelopathy can miss spinal cord disease.
Board Question
A 29-year-old woman develops rapidly progressive bilateral leg weakness, a sensory level at the umbilicus, and urinary retention over 24 hours. She is afebrile and has no trauma history. MRI shows no epidural abscess or mass. What is the best next treatment?
AHigh-dose IV methylprednisolone
BOral gabapentin and discharge
CLumbar puncture before any treatment
DIV ceftriaxone and vancomycin only
Reveal answer
Correct: A
With compressive causes excluded and an acute inflammatory myelopathy pattern, high-dose IV steroids are the standard ED-started therapy. LP and further etiologic testing are important, but they follow exclusion of emergencies that require surgery or antibiotics.
Practical review of acute transverse myelitis workup and treatment, emphasizing MRI spine/brain, CSF and antibody testing, exclusion of compressive lesions, and early high-dose steroids with escalation to plasma exchange when severe or ster
3 of 4
Myasthenia Gravis
Myasthenia gravis can present as fluctuating weakness but suddenly become a respiratory emergency. The ED job is to recognize impending crisis, avoid...
A 72-year-old man clears his throat repeatedly between short, frustrated sentences, the sound dry and weak in the exam room. His eyelids sink as the afternoon stretches on; by the time you ask him to count to twenty, his voice has thinned to a whisper. He can smile on command, but after a few seconds the grin collapses and his jaw seems to tire. The monitor is fine, the lungs are still moving air, and yet the danger is already in motion — you just haven’t measured it yet.
Before You Read
What bedside finding tells you this weakness is neuromuscular junction failure?
How do you decide who is in impending respiratory crisis?
Which ED meds help, which hurt, and which can tip the patient into failure?
Why It Matters
Myasthenia gravis can present as fluctuating weakness but suddenly become a respiratory emergency. The ED job is to recognize impending crisis, avoid iatrogenic worsening, and start targeted treatment while protecting ventilation.
When to Think of It
Think MG with fatigable, fluctuating weakness: ptosis, diplopia, dysarthria, dysphagia, chewing fatigue, neck weakness, or proximal limb weakness that worsens with repetition and improves with rest. Pupils and sensation are typically spared, which helps distinguish it from many other neurologic disorders.
Sick or Not Sick
The fork is impending respiratory failure vs. stable weakness. If the patient cannot count, has weak cough, pooling secretions, accessory muscle use, single-breath count is low, or bedside spirometry shows declining FVC/NIF, treat as crisis and prepare for airway support.
The First Fifteen Minutes
Respiratory compromise or bulbar dysfunction → airway-first assessment, continuous pulse ox/capnography, and intubation readiness because weakness can decompensate abruptly.
Impending crisis or severe generalized weakness → admit to ICU/stepdown depending on respiratory metrics; if intubation is needed, use standard RSI dosing per institutional protocol.
Known or suspected MG exacerbation without crisis → pyridostigmine 30–60 mg PO q4–6h may be continued or started if swallowing is safe, because it improves neuromuscular transmission.
Moderate/severe exacerbation → corticosteroids often used, but may transiently worsen weakness at initiation; coordinate with neurology. Common ED bridge if not intubated is prednisone 40–60 mg PO daily or equivalent, but confirm with neurology because practice varies.
Trigger search and treatment → evaluate for infection, medication trigger, and electrolyte derangement; if infection suspected, treat it because infection is a common precipitant of crisis.
If clear myasthenic crisis or severe bulbar/respiratory weakness → IVIG 2 g/kg divided over 2–5 days or plasmapheresis inpatient, because they provide rapid short-term improvement.
Admit most symptomatic patients; ICU for crisis, intubation, or borderline respiratory metrics. Neurology should guide antibody testing, chest imaging for thymoma, and longer-term immunotherapy. Avoid medications that worsen neuromuscular transmission when possible, and reconcile home pyridostigmine carefully. If swallowing is unsafe, keep NPO and use enteral/IV alternatives as appropriate.
How This One Kills
The classic disaster is assuming “just fatigue” and sending home a patient whose bulbar weakness is marching toward respiratory collapse. Another miss is giving a drug that worsens MG, then mistaking iatrogenic decline for disease progression.
The Atypical Presentation
Older adults may present with isolated dysphagia, neck weakness, or “recurrent aspiration” rather than dramatic diplopia. Some patients only look worse late in the day, after exertion, or during infection, making the exam seem deceptively normal early. If the story is fluctuating and sensory exam is clean, ask about chewing, counting aloud, and fatigability rather than waiting for obvious paralysis.
Back to Our Patient
Back to our 72-year-old with ptosis, weak voice, and fatigable smile: this is classic myasthenia gravis with possible bulbar involvement, and the immediate question is whether he can protect his airway. He needs respiratory assessment now, including bedside spirometry if available, plus trigger evaluation for infection or medication exposure. If he is borderline or worsening, admit to ICU and prepare for intubation; if stable enough to swallow, continue or start pyridostigmine and involve neurology early for IVIG or steroids as indicated.
Patient Presentation to Attending
“72-year-old man with known/possible myasthenia presenting with fluctuating ptosis, dysarthria, and chewing fatigue that worsens over the course of the day. He has no sensory loss, no pupil involvement, and no focal UMN signs, which makes stroke less likely; the main concern is bulbar weakness with possible impending respiratory failure. He’s able to speak only short phrases and has a weak cough, so I’m getting FVC/NIF, continuous monitoring, and preparing airway backup. I’ve started a trigger search for infection and medication exposures, and I’m calling neurology for ICU-level management and consideration of IVIG/plasma exchange.”
Study Directive
Practice a 2-minute MG crisis assessment: speech, cough, secretion handling, FVC/NIF, neck flexion.
Make a “meds that worsen MG” flash list and review it daily.
Memorize a simple disposition rule: bulbar symptoms or low respiratory metrics = ICU.
Rehearse a one-line oral presentation distinguishing MG vs. GBS vs. stroke.
Review local protocol for IVIG vs plasmapheresis and steroid bridging.
Key Medications
Pyridostigmine 30–60 mg PO q4–6h.
Prednisone 40–60 mg PO daily as a common bridge; exact dosing/taper varies.
Atropine 0.5–1 mg IV PRN for significant secretions/bradycardia from cholinergic excess, not routine MG treatment. Airway/RSI medication selection in MG is high-stakes and institution-dependent; check a reference if uncertain.
High-Yield Pearls
Normal SpO₂ does not rule out neuromuscular respiratory failure.
A clean sensory exam with fatigable weakness points toward MG, not neuropathy.
New dysphagia in MG is a crisis warning sign, not a minor symptom.
The Mimics
Guillain-Barré syndrome — ascending weakness and areflexia rather than fatigable ocular/bulbar weakness; confusing it risks missing MG crisis vs. neuropathy.
Botulism — prominent autonomic symptoms and fixed dilated pupils; confusing it with MG can delay antitoxin.
Stroke/brainstem lesion — abrupt focal deficits and UMN signs; confusing it with MG can miss CNS catastrophe.
Lambert-Eaton syndrome — strength improves with use and autonomic symptoms are prominent; confusing it with MG changes the malignancy search and treatment.
Board Question
A 68-year-old woman with known myasthenia gravis presents with worsening dysphagia, weak cough, and shortness of breath. She can speak only a few words at a time and has pooling secretions. What is the best next step?
AReassure and discharge if oxygen saturation is normal
BGive pyridostigmine only and observe in the waiting room
CPrepare for airway management and admit for crisis-level care
DPerform lumbar puncture to confirm the diagnosis
Reveal answer
Correct: C
Bulbar weakness and weak cough are signs of impending respiratory failure in myasthenia gravis, even if oxygenation is initially normal. The priority is airway readiness and ICU-level monitoring, with disease-directed therapy coordinated after stabilization.
A current broad review useful for ED framing of fluctuating weakness, ocular/bulbar symptoms, respiratory crisis risk, diagnostic testing, and acute immunomodulatory options such as IVIG or plasma exchange.
4 of 4
Primary Headache
Primary headache is common, but dangerous secondary headaches are less common and easy to miss if you anchor too early. The ED goal is to identify red...
A 27-year-old woman lies under the exam-room lights with sunglasses still on, one hand pressed to her temple while the other scrolls through a phone she can barely tolerate. The coffee she left in the lobby has gone cold; she winces at the hum of the monitor and says the pain is “the same one,” just louder now, with nausea and a need for darkness. Her neuro exam is normal, her vitals are calm, and the real work is deciding whether this is the familiar face of headache — or the one that hides something worse.
Before You Read
When is a headache primary, and when is it a secondary emergency until proven otherwise?
Which bedside features actually discriminate migraine, tension, and cluster?
What ED treatments relieve pain fast without masking a dangerous mimic?
Why It Matters
Primary headache is common, but dangerous secondary headaches are less common and easy to miss if you anchor too early. The ED goal is to identify red flags, treat the pain effectively, and avoid unnecessary testing in the right patient.
When to Think of It
Think primary headache when there is a recurrent pattern, normal neurologic exam, no thunderclap onset, no fever/meningismus, no trauma, no papilledema, and no focal deficit. Migraine, tension-type headache, and cluster headache dominate the primary headache spectrum.
Sick or Not Sick
The fork is red flags for secondary headache vs. a stable recurrent primary syndrome. Thunderclap onset, first/worst headache, age >50 with new headache, immunosuppression, pregnancy/postpartum, exertional onset, neurologic deficit, altered mental status, papilledema, or anticoagulation should override the “primary” label.
The First Fifteen Minutes
Migraine phenotype → ketorolac 15–30 mg IV, because NSAID analgesia targets inflammatory pain pathways.
Migraine with nausea/poor PO → metoclopramide 10 mg IV or prochlorperazine 10 mg IV, because dopamine antagonism treats both pain and nausea.
Migraine with severe refractory pain → add diphenhydramine 25 mg IV to reduce akathisia when using dopamine antagonists; not an analgesic by itself.
Cluster headache → high-flow oxygen via nonrebreather 12–15 L/min for 15–20 min and sumatriptan 6 mg SQ, because vasoconstriction and trigeminal modulation abort attacks quickly.
Severe dehydration/vomiting → 1 L normal saline or balanced crystalloid IV, because volume depletion worsens migraine and medication tolerance.
Avoid routine opioids; if truly needed after first-line failure, use sparingly because they worsen recurrence and return visits.
Dosing for certain rescue agents (e.g., valproate, magnesium, dexamethasone) varies by institution; check a reference if uncertain.
Definitive Care & Disposition
Primary headache disposition is usually discharge with a clear diagnosis, response to therapy, return precautions, and outpatient follow-up. Add dexamethasone or a migraine rescue plan when appropriate to reduce recurrence per local practice. Cluster patients need neurology follow-up and home abortive therapy planning; recurrent or disabling headaches deserve preventive strategy discussion.
How This One Kills
The dangerous miss is calling a secondary headache “migraine” because the neuro exam is normal early. The other common failure is under-treating a true primary headache, which drives bounce-backs and diagnostic drift.
The Atypical Presentation
Older adults may call a new secondary headache “my usual migraine,” especially if they have a headache history. Pregnant and postpartum patients can present with headache that looks migrainous but actually reflects preeclampsia, cerebral venous thrombosis, or hemorrhage. In kids, headache may be described as abdominal pain, irritability, or visual complaints, so don’t rely on adult-style descriptors alone.
Back to Our Patient
Back to our 27-year-old with the same recurrent, dark-room headache, nausea, and normal exam: this fits a primary headache, most likely migraine, once red flags are excluded. She is not toxic, has no neurologic deficit, and has a prior similar pattern, so the move is symptom control with an anti-inflammatory plus antiemetic, reassessment, and discharge if she improves and can hydrate. If she fails first-line therapy or develops any red flag features, the diagnosis must be reopened before calling it “just migraine.”
Patient Presentation to Attending
“27-year-old woman with recurrent unilateral throbbing headache, photophobia, nausea, and prior similar episodes, now worse over the last day but without thunderclap onset. She has a normal neuro exam, no fever, no neck stiffness, no trauma, no papilledema, and no focal deficits. This is most consistent with primary headache, likely migraine, and I don’t see secondary red flags right now. I’ve given ketorolac and metoclopramide, will reassess response, and if she improves she can discharge with return precautions and outpatient follow-up.”
Study Directive
Make a red-flag checklist from memory: SNOOP/SNNOOP-ish and recite it daily.
Practice differentiating migraine vs cluster vs tension in 30 seconds from a vignette.
Build a simple ED migraine order set and know the doses cold.
Review when headache needs CT, LP, MRI, or none.
Write one discharge plan that includes rescue meds, hydration, and follow-up for recurrent migraine.
---
Mechanism Pearl of the Day: Across spinal infection, inflammatory myelitis, and myasthenic crisis, the same ED danger is function failing before the anatomy is obvious: pain may precede compression, weakness may precede respiratory collapse, and bladder symptoms may precede irreversible cord injury. In the headache patient, the analogous trap is assuming a familiar symptom pattern means a benign mechanism when the history has already shifted away from the expected pattern.
Key Medications
Ketorolac 15–30 mg IV/IM once.
Metoclopramide 10 mg IV.
Prochlorperazine 10 mg IV.
Diphenhydramine 25 mg IV.
Sumatriptan 6 mg SQ once; oral/nasal forms vary.
Oxygen 12–15 L/min nonrebreather for cluster headache.
A normal neuro exam reduces but does not eliminate secondary headache risk; the history does the heavy lifting.
Cluster headache patients look miserable and restless, not quiet and dark-room-seeking like many migraine patients.
Treating migraine early with effective non-opioid therapy reduces bounce-backs and diagnostic anchoring.
The Mimics
Subarachnoid hemorrhage — thunderclap onset and exertional peak; confusing it with migraine can be fatal.
Meningitis/encephalitis — fever, meningismus, or altered mental status; missing it delays antibiotics/antivirals.
Idiopathic intracranial hypertension — papilledema and positional headache in the right demographic; confusing it with migraine misses vision-threatening disease.
Intracerebral hemorrhage — focal deficits, severe hypertension, or acute neurologic change; missing it delays emergent neuroimaging.
Board Question
A 24-year-old woman with a long migraine history presents with unilateral throbbing headache, photophobia, and nausea. She is afebrile, has a normal neurologic exam, and has had similar episodes before. What is the most appropriate ED treatment?
AImmediate lumbar puncture
BKetorolac plus a dopamine antagonist
CEmergent CT angiography of the head and neck for all patients
DHigh-dose steroids as first-line therapy
Reveal answer
Correct: B
This is a typical migraine presentation without red flags, so parenteral NSAID plus antiemetic therapy is appropriate. LP and vascular imaging are reserved for secondary headache concerns based on red flags or exam findings.
A broad, practical reference for ED headache visits: use red flags to separate secondary causes, then treat common primary headaches with evidence-based acute therapy such as NSAIDs/acetaminophen, dopamine-antagonist antiemetics or triptans
Yesterday’s Differential
The daily puzzle — from editions past
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
An 82-year-old man presents with weakness and near-syncope. The ECG shows P waves marching through at 80 bpm while the QRS complexes appear independently at 32 bpm. What’s the diagnosis, and the first move?
Check your answer
AV Block — Third Degree / Complete Heart Block. If unstable, start ACLS bradycardia management: pads on, atropine if appropriate, transcutaneous pacing, pressor infusion, and cardiology for transvenous pacing. Treat reversible causes in parallel.
From the June 22 edition
Today, three days ago: Sodium Bicarbonate. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
TCA/sodium-channel blocker toxicity: 1–2 mEq/kg IV bolus, repeat to narrow QRS and target pH ~7.45–7.55, then infusion. Hyperkalemia/acidosis: often 50 mEq IV bolus when indicated. Severe alkalemia, hypocalcemia-related tetany, sodium/volume overload caution.
From the June 15 edition
A 33-year-old man has a stab wound to the lateral neck. He is hemodynamically stable, has no active bleeding, but reports dysphagia and mild hoarseness. Exam shows a small wound that appears to violate the platysma, but no expanding hematoma or neurologic deficit. What is the best next step?
ADischarge with oral antibiotics and return precautions
BBlindly probe the wound to determine depth
CCT angiography of the neck with trauma surgery consultation
DImmediate neck exploration in the OR without imaging
Reveal answer
Correct · C
In a stable patient without hard signs, CTA neck is the usual first-line evaluation when the platysma is violated. Dysphagia and hoarseness raise concern for aerodigestive injury, so imaging plus specialty consultation is appropriate; blind probing is dangerous, and immediate OR is reserved for hard signs or instability.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Shift pearls returns with urinary obstruction in septic shock. The post Shift Pearls: Anatomic Urinary Obstruction and Septic Shock appeared first on emDocs .
Persistent postoperative sore throat could signal a rare intubation complication. Learn how to spot uvular necrosis in your emergency department. The post Case Report: When Sore Throat Is More Than Just a Pain in the Neck appeared first on ACEP Now .
In this episode, Sam Ashoo, MD and Dr. T.R. Eckler, MD discuss the April 2026 Emergency Medicine Practice article, Wide Complex Tachycardia in the Emergency Department: An Updated Approach to Diagnosis and Management . Introduction – 0:11 Article Overview – 2:02 Top 5 Bedside Steps – 7:54 Sodium Channel Blockade – 9:26 Hyperkalemia – 11:53 SVT with...
AHA Guidelines and some new studies strengthen the EMCrit recs for Sick PE management EMCrit Project by Scott Weingart, MD FCCM .
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
Cephalexin
First-generation cephalosporin
Indication
Outpatient non-purulent cellulitis and other MSSA/streptococcal SSTI, streptococcal pharyngitis, uncomplicated cystitis, and impetigo. Not MRSA-active.
What’s your dose? — reveal dosing & cautions
ED Dose
500 mg PO q6h (q12h for milder infections). Cellulitis: 500 mg PO QID. Strep pharyngitis: 500 mg PO BID x10 days. Pediatric: 25–50 mg/kg/day divided q6–12h.
Renal Adjustment
Reduce dose/frequency in CrCl < 30 mL/min (e.g. extend interval). HD: dose after dialysis.
Contraindications
Cephalosporin hypersensitivity. Use caution with documented severe (anaphylactic) penicillin allergy, though cross-reactivity with first-generation cephalosporins is low.
Interactions
Probenecid increases levels; metformin concentrations may rise.
Monitoring
Clinical response, GI tolerance; renal function in CKD.
ED Pearl
Covers MSSA and strep but NOT MRSA — a purulent abscess or cellulitis needs MRSA coverage (TMP-SMX or doxycycline), not cephalexin alone.
Trauma with significant hemorrhage within 3 h of injury; postpartum hemorrhage; severe epistaxis; menorrhagia; perioperative bleeding.
What’s your dose? — reveal dosing & cautions
ED Dose
Trauma: 1 g IV over 10 min, then 1 g IV over 8 h (CRASH-2 protocol). Postpartum hemorrhage: 1 g IV over 10 min within 3 h, may repeat once. Topical/nebulized for epistaxis or hemoptysis.
Renal Adjustment
CrCl 50–80: 10 mg/kg q12h (chronic dosing). CrCl < 30: avoid or use markedly reduced dose. Trauma loading dose generally given regardless.
Contraindications
Active intravascular thrombosis or thromboembolic disease; subarachnoid hemorrhage (relative — risk vs benefit); known hypersensitivity.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Rhythm
Polymorphic VT
Polymorphic VT is a malignant ventricular rhythm; QT status separates torsades from ischemic polymorphic VT.
The Tracing
A 63-year-old man with crushing chest pain has repeated runs of wide-complex tachycardia with changing QRS morphology and axis. Between episodes, the QT interval is not prolonged, but there is anterior ST depression with aVR elevation. A second patient on methadone has similar twisting VT but a QTc of 610 ms. Same rhythm family, different treatment priorities.
Wide-complex tachycardia with beat-to-beat variation in QRS morphology and axis
May be sustained or nonsustained; can degenerate into VF
QT prolongation suggests torsades de pointes
Normal QT polymorphic VT suggests acute ischemia or scar-related electrical instability
Often presents with syncope, shock, chest pain, or cardiac arrest
Pearls
Always ask: polymorphic VT with long QT, or polymorphic VT with normal QT? The answer changes the next medication and trigger hunt.
Ischemic polymorphic VT is a cath-lab problem as much as an antiarrhythmic problem.
Defibrillation is the treatment when pulseless or unstable; do not overthink morphology during arrest.
Pitfalls
Do not reflexively give magnesium and stop thinking; magnesium is key for torsades, but ischemic PMVT needs ischemia treatment.
Do not use synchronized cardioversion when the rhythm is too chaotic to sync reliably; defibrillate if unstable/pulseless.
Do not miss QT-prolonging meds and electrolytes after the rhythm terminates.
At the Bedside
If unstable or pulseless, defibrillate. If perfusing, determine QT status, correct electrolytes, treat ischemia aggressively, and use expert-guided antiarrhythmic therapy based on suspected mechanism.
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 · Infections of the Spinal Column
Self-Examination
Test Your Understanding
A 61-year-old man with diabetes presents with 5 days of worsening thoracic back pain, fever, and difficulty walking. Exam shows midline spine tenderness and new bilateral leg weakness; bladder scan reveals 700 mL urinary retention. Which is the next best step?
ANSAIDs and outpatient physical therapy
BEmergent MRI of the spine with IV contrast
CLumbar puncture before antibiotics
DReassurance and repeat exam in 24 hours
Reveal answer
Correct answer · B
This patient has red flags for spinal infection with cord/cauda equina compromise, so urgent MRI with contrast is the key diagnostic step. In parallel, blood cultures and empiric IV antibiotics should be started promptly, but imaging and spine consultation cannot wait.
Study Pace4 topics today; 76 remaining; Day 24 of 43Deadline · June 1, 2026