An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Aneurysmal Subarachnoid Hemorrhage
Aneurysmal SAH kills early from rebleeding and later from delayed ischemia. Missing it means sending home a patient whose second bleed may be the fatal one.
A 49-year-old woman leans over the triage desk, one hand pressed to her temple, the other gripping her phone so tightly her knuckles blanch. She says the headache hit “like a gunshot” while she was folding laundry, and now the fluorescent lights make her eyes sting. Nausea keeps rolling through her, and she keeps asking for the curtain to be closed because the room feels too bright. She can answer questions, but every minute she looks more uncomfortable, and the monitor shows a blood pressure that is higher than you’d like. You have not yet decided whether this is just a bad migraine or something that will not wait.
— What’s your move? Read on.
Before you read
What is the one immediate management fork that changes everything?
Which medication buys time, and which intervention actually prevents rebleeding?
When to Think of It
Thunderclap headache reaching maximal intensity in seconds to minutes, especially with exertional onset, vomiting, meningismus, photophobia, syncope, seizure, or transient loss of consciousness. Enter this diagnosis early even if the neuro exam is normal.
Sick or Not Sick
The single call: is she neurologically intact and hemodynamically stable enough for urgent imaging/transfer, or is she deteriorating and needs airway/ICP-focused resuscitation now? Hunt-Hess/WFNS severity matters, but the practical fork is “can she protect brain perfusion and get to definitive aneurysm care safely?”
The First Fifteen Minutes
Severe pain, vomiting, agitation → fentanyl 25–50 mcg IV q5–10 min PRN for analgesia; ondansetron 4–8 mg IV for emesis, because pain/vomiting spike BP and ICP.
SBP persistently elevated (commonly >160 mm Hg while aneurysm unsecured) → nicardipine 5 mg/h IV, titrate by 2.5 mg/h every 5–15 min (max 15 mg/h) or clevidipine 1–2 mg/h IV, double every 90 sec initially to effect because controlled reduction lowers rebleed risk without crashing CPP.
Concern for seizures or witnessed seizure → levetiracetam 1,000–1,500 mg IV now (then maintenance per protocol), because early seizure worsens ICP and oxygen demand.
If declining mental status, aspiration risk, or inability to protect airway → rapid sequence intubation with induction/paralysis per your usual ED protocol, because hypoxia/hypercarbia rapidly worsen cerebral blood flow and ICP.
Suspected raised ICP with impending herniation → hypertonic saline 3% 2–3 mL/kg IV bolus (or institutional equivalent) because osmotic therapy can transiently lower ICP.
If hypotensive or volume depleted → isotonic crystalloid bolus (e.g., 500–1,000 mL normal saline) because cerebral perfusion is pressure dependent; avoid hypotonic fluids.
Definitive Care & Disposition
Noncontrast head CT first; if negative but suspicion remains high and timing is appropriate, proceed to LP or CTA per local pathway and risk tolerance. Once diagnosed, give nimodipine 60 mg PO/NG q4h as early as possible if enteral route is available, because it reduces delayed ischemic deficits. Neurosurgery/neurocritical care consultation is mandatory; transfer to a center with aneurysm coiling/clipping if not available. Admit to ICU or neuro-ICU; unsecured aneurysm = close BP control, frequent neuro checks, and expedited aneurysm occlusion.
How This One Kills
The catastrophic failure is treating it like a benign headache and missing the unsecured aneurysm—the patient rebleeds in the hours after discharge or during a blood pressure surge, often before definitive care is reached.
The Differential — What Else Looks Like This
Migraine — usually has a recurrent pattern, aura/photophobia history, and slower escalation; confusing it with SAH misses the rebleed window.
Meningitis — fever and infectious prodrome point away; confusing it delays aneurysm imaging and BP control.
Cervical artery dissection — neck pain or focal deficit may dominate; missing SAH means chasing the wrong vascular lesion.
Sentinel headache / benign thunderclap — CT can be negative early; assuming benignity without follow-up workup risks missing the leak before rupture.
The Second-Day Story
Older patients, patients with limited pain expression, and those who present late may not volunteer “worst headache of life.” Some have only sudden occipital pain, vomiting, neck pain, or brief collapse; others are nearly neurologically intact except for photophobia or a markedly unusual headache. If the story sounds abrupt and maximal at onset, do not let a normal exam or mild improvement after analgesia reassure you out of the diagnosis.
Back to Our Patient
Back to our 49-year-old woman with the lightning-onset headache and photophobia: this is aneurysmal subarachnoid hemorrhage until proven otherwise. She needs emergent noncontrast head CT, BP control with nicardipine if SBP remains high, antiemetic and analgesia to blunt ICP surges, and urgent neurosurgery/neurocritical care involvement for aneurysm securing. If the CT is negative but suspicion remains high, the workup continues rather than stopping at “migraine.” She goes to ICU-level care and definitive aneurysm management, not home.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“49-year-old woman with sudden severe headache that began explosively while folding laundry, now with photophobia and nausea, no prior similar headaches, and no focal weakness or trauma. She’s alert but very uncomfortable, with a nonfocal neuro exam and BP 178/96. I’m concerned for aneurysmal subarachnoid hemorrhage. I’ve kept her NPO, started antiemetic and analgesia, and I’m getting an emergent noncontrast head CT now with neurosurgery alerted. If CT is negative and suspicion remains, I’ll pursue the next diagnostic step rather than stopping.”
Study Directive
Draw the SAH workflow from memory: thunderclap headache → CT → LP/CTA if needed → BP control → nimodipine → ICU/neurosurgery.
Practice three “can’t miss” opening questions for sudden headache: onset timing, maximal intensity timing, and associated collapse/vomiting/neck stiffness.
Memorize nimodipine dosing and one alternative BP infusion each for neuro-bleed patients.
Review 5 CT/LP decision pathways and decide when your shop uses LP versus CTA after negative CT.
Hoh BL, Ko NU, Amin-Hanjani S, et al. · Stroke, 2023 · PMID 37212182 · cited 924×
The current AHA/ASA guideline anchors ED priorities after suspected or confirmed aneurysmal SAH: rapid diagnosis, early neurovascular consultation/transfer, blood pressure control, anticoagulant reversal, nimodipine, hydrocephalus managemen
Cervical artery dissection is a major cause of stroke in younger adults. The first presentation may be pain alone, but the next event can be embolic infarct.
A 36-year-old man walks in rubbing the left side of his neck, his baseball cap still damp from a pickup game in the heat. He says the pain started after he turned his head hard to catch a ball, and now the ache runs up behind his ear into a headache that feels “wrong” in a way he can’t explain. He noticed his eyelid looks a little droopy in the mirror, and his vision seems off when he looks into the distance. He is speaking normally, but the story feels too clean to dismiss and too odd to label a strain. You have not yet decided whether the neck pain is the whole story.
Before You Read
What bedside clue should make you think artery dissection, not muscle strain?
Which deficit pattern suggests carotid versus vertebral dissection?
What is the safest immediate ED path before vascular imaging confirms it?
Why It Matters
Cervical artery dissection is a major cause of stroke in younger adults. The first presentation may be pain alone, but the next event can be embolic infarct.
When to Think of It
Unilateral neck pain or headache after minor trauma, sudden neck rotation/manipulation, chiropractic manipulation, coughing/vomiting, or connective tissue disease; plus Horner syndrome, transient neuro deficits, posterior circulation symptoms, or retinal ischemic symptoms.
Sick or Not Sick
The key fork is “pain only” versus “pain plus ischemic signs or evolving deficits.” Any focal neurologic deficit, transient ischemic attack, or visual/brainstem symptom makes this a stroke-pathway patient, not simple musculoskeletal neck pain.
The First Fifteen Minutes
Focal deficit / stroke concern within window → activate stroke evaluation and obtain CTA head/neck now because diagnosis changes antithrombotic planning and reperfusion eligibility.
Pain control → acetaminophen 650–1,000 mg PO/IV or fentanyl 25–50 mcg IV q5–10 min PRN because analgesia reduces sympathetic surge and patient distress.
If hypertensive and not having perfusion-dependent deficits → treat per stroke/vascular protocol; avoid abrupt overcorrection because cerebral perfusion may be pressure sensitive.
If large-vessel occlusion suspected → coordinate with stroke team for reperfusion decisions; no empiric thrombolysis decisions outside the stroke algorithm.
Definitive Care & Disposition
CTA head/neck is the usual ED test; MRI/MRA can help when CTA is nondiagnostic. Antithrombotic therapy is individualized by stroke neurology—either antiplatelet or anticoagulation is commonly used after hemorrhage is excluded and depending on infarct burden, vessel features, and institutional practice. Admit if ischemic symptoms, significant pain with uncertain follow-up, or imaging-proven dissection; discharge is uncommon unless diagnosis is excluded and symptoms are clearly benign. Consult neurology/stroke early.
How This One Kills
The failure mode is mislabeling the pain as a sprain and missing the embolic stroke that follows hours to days later.
The Atypical Presentation
Some patients present with only unilateral head/neck pain and no deficits, especially early. Others show isolated Horner syndrome, transient monocular vision loss, vertigo, or brief posterior circulation symptoms that resolve before evaluation. If the pain is new, unilateral, and linked to a minor mechanical trigger, keep dissection high even when the exam is almost normal.
Back to Our Patient
Back to our 36-year-old after the pickup game: the unilateral neck pain, post-rotation onset, and subtle Horner-like eye change should trigger cervical artery dissection. He needs CTA head and neck, stroke-team involvement, and careful neurologic reassessment rather than a discharge diagnosis of strain. If imaging confirms dissection, secondary stroke prevention is started after hemorrhage is excluded and disposition is usually admission. The key is that the neck pain was the warning shot, not the whole injury.
Patient Presentation to Attending
“36-year-old man with new unilateral neck pain and headache after forceful head rotation during a pickup game, now with subtle left eyelid droop and visual discomfort, no trauma major enough to explain it, and no arm weakness or speech change. Exam is largely nonfocal except for the possible Horner feature, and he is hemodynamically stable. I’m concerned for cervical artery dissection with possible evolving ischemia. I’ve given analgesia, am getting CTA head and neck now, and have alerted stroke neurology in case there’s an infarct or large-vessel issue.”
Study Directive
Memorize the dissection trigger list: minor trauma, rotation, chiropractic manipulation, coughing/vomiting, connective tissue disease.
Sketch carotid versus vertebral symptom patterns from memory.
Practice a one-minute CTA head/neck indication script for young patient + unilateral neck pain.
Review your local stroke pathway for antiplatelet vs anticoagulation decisions after dissection.
Key Medications
Acetaminophen: 650–1,000 mg PO/IV q6h PRN; max daily dose per liver risk.
Fentanyl: 25–50 mcg IV q5–10 min PRN.
Aspirin: 160–325 mg PO chew once when ischemic stroke is suspected and hemorrhage has been excluded; coordinate with stroke team.
Anticoagulation/other antithrombotic therapy: varies by neurology/stroke protocol; check local guidance and imaging specifics.
Thrombolysis or thrombectomy-related meds: stroke-pathway dependent, not dissection-specific.
High-Yield Pearls
Pain-only dissections exist; the story can be the only clue before stroke appears.
Horner syndrome with neck pain is carotid dissection until proven otherwise.
The worst mistake is reassuring yourself because the neuro exam is currently normal.
The Mimics
Muscle strain — pain worsens with movement but lacks Horner syndrome or neuro symptoms; confusing it delays stroke workup.
Migraine with aura — can cause headache and visual symptoms, but neck pain after trauma/manipulation is the tell; missing dissection risks infarct.
Acute ischemic stroke from another cause — dissection often has preceding neck pain/headache; missing the vessel source can change secondary prevention.
Aortic dissection — chest/back pain and pulse deficits dominate; mixing them up can send you to the wrong imaging territory.
Board Question
A 29-year-old woman presents with unilateral neck pain and headache after a chiropractic neck manipulation. She has ptosis and miosis but no weakness. Which diagnosis is most likely?
ACervical artery dissection
BTension headache
CBell palsy
DTemporal arteritis
Reveal answer
Correct: A
Cervical artery dissection. Unilateral neck pain after minor trauma or manipulation plus Horner syndrome is classic for carotid dissection. Tension headache does not cause focal sympathetic findings, Bell palsy causes facial weakness, and temporal arteritis is unusual at this age and does not fit the trigger.
AHA scientific statement is the best bedside reference for recognizing suspected carotid/vertebral dissection, choosing vascular imaging, and coordinating acute stroke and antithrombotic management.
STOP-CAD provides large multicenter real-world data on anticoagulation versus antiplatelet therapy after cervical artery dissection, informing the ED handoff decision when dissection is diagnosed without a clear thrombolysis or thrombectomy
ICH has high early mortality and neurologic injury worsens with hematoma expansion. Speed matters because blood pressure, coagulopathy, and mass effect are...
A 71-year-old man arrives slumped in the wheelchair, a half-finished coffee cooling in his hand and a smear of toothpaste still on his chin. His wife says he suddenly “stopped making sense” while shaving, and now his right arm hangs uselessly while he tries to answer with slurred, frustrated words. The monitor shows a sky-high blood pressure, and he keeps drifting between agitation and confusion. The room has that tense, narrow feel of a time-sensitive disaster, but the diagnosis has not yet been named.
Before You Read
What differentiates ICH from ischemic stroke at the bedside before the scan?
What is the most important immediate management target after hemorrhage is seen?
Which therapies help, and which common stroke treatments become dangerous?
Why It Matters
ICH has high early mortality and neurologic injury worsens with hematoma expansion. Speed matters because blood pressure, coagulopathy, and mass effect are the modifiable threats.
When to Think of It
Sudden focal deficit with headache, vomiting, decreased level of consciousness, severe hypertension, seizure, or rapid deterioration. Think hemorrhage especially in older patients, anticoagulated patients, and those with small-vessel risk factors.
Sick or Not Sick
The single call: is there airway/brainstem compromise, mass effect, or anticoagulant-associated hemorrhage? Those findings push toward ICU-level resuscitation, emergent reversal, and neurosurgical consideration.
The First Fifteen Minutes
Airway threat / low GCS / aspiration risk → RSI per protocol because hypoxia and hypercarbia worsen secondary brain injury.
Severe hypertension with ICH → nicardipine 5 mg/h IV, titrate by 2.5 mg/h every 5–15 min to goal per protocol or clevidipine 1–2 mg/h IV because controlled lowering can limit hematoma expansion.
Warfarin-associated ICH → 4-factor PCC 50 units/kg IV (max per product/protocol) + vitamin K 10 mg IV because rapid factor replacement and durable reversal stop expansion.
Dabigatran-associated ICH → idarucizumab 5 g IV because it reverses thrombin inhibition quickly.
Factor Xa inhibitor-associated ICH → andexanet alfa per institutional dosing protocol, or 4-factor PCC when andexanet is unavailable/contraindicated because reversal may reduce ongoing bleeding; dosing varies significantly.
Elevated ICP/herniation concern → hypertonic saline 3% 2–3 mL/kg IV bolus because osmotic therapy temporarily lowers ICP.
Pain/agitation/nausea → fentanyl 25–50 mcg IV PRN; ondansetron 4–8 mg IV because sympathetic surges can worsen BP and ICP.
Definitive Care & Disposition
Noncontrast CT confirms the bleed; CTA/CTV or MRI may follow to look for cause in selected cases. All spontaneous ICH needs neurology/neurosurgery involvement, strict BP strategy, coagulation reversal when indicated, and ICU or neuro-ICU admission. Neurosurgical evacuation is case-dependent, usually for cerebellar hemorrhage, obstructive hydrocephalus, or life-threatening mass effect; external ventricular drain may be needed. Avoid routine anticoagulants/antiplatelets until a specialist-directed plan is in place.
How This One Kills
The failure mode is leaving anticoagulation un-reversed or assuming the deficit is ischemic and giving the wrong stroke pathway treatment, allowing the hematoma to enlarge.
The Atypical Presentation
Small hemorrhages can look like mild confusion, isolated aphasia, or a “bad stroke” with little pain. Elderly patients and those on anticoagulants may present after a fall, with nonspecific weakness, or with reduced consciousness rather than a dramatic focal deficit. When the exam is cloudy and BP is severe, scan early and trust the image more than the story.
Back to Our Patient
Back to our 71-year-old with abrupt aphasia, right arm weakness, and severe hypertension: this is intracerebral hemorrhage until the CT says otherwise. He needs an emergent noncontrast head CT, airway protection if his mental status worsens, BP control with nicardipine, and reversal if he is anticoagulated. If the scan shows hemorrhage, neurology/neurosurgery and ICU-level admission follow immediately, with further imaging only if needed to define cause. The priority is preventing expansion and secondary injury, not chasing ischemic stroke therapies.
Patient Presentation to Attending
“71-year-old man with abrupt aphasia and right arm weakness that started while shaving, now confused with severe hypertension and fluctuating attention, no clear seizure activity, and no major trauma. Exam shows dense right arm drift and dysarthria, and he’s been becoming less reliable with commands. I’m worried about intracerebral hemorrhage versus ischemic stroke, but the blood pressure and encephalopathy make hemorrhage particularly concerning. I’ve placed him on monitors, am getting an emergent noncontrast head CT, and if hemorrhage is confirmed I’ll start BP control and reverse anticoagulation if present while involving neurology and neurosurgery.”
Study Directive
Drill the anticoagulant reversal algorithm from memory: warfarin, dabigatran, factor Xa inhibitor.
Practice reading a one-sentence ICH presentation and immediately naming the first three actions.
Draw a “hemorrhagic vs ischemic stroke” bedside comparison list from memory.
Confirm your institution’s preferred nicardipine/clevidipine and reversal pathways.
Key Medications
Nicardipine: 5 mg/h IV, titrate by 2.5 mg/h every 5–15 min to goal.
Clevidipine: 1–2 mg/h IV, titrate per response.
4-factor PCC: 50 units/kg IV for warfarin reversal; check product max/protocol.
Vitamin K: 10 mg IV slow infusion for warfarin reversal.
Idarucizumab: 5 g IV for dabigatran reversal.
Andexanet alfa: dosing depends on DOAC, last dose, and timing; verify protocol.
Hypertonic saline 3%: 2–3 mL/kg IV bolus.
Fentanyl: 25–50 mcg IV PRN.
Ondansetron: 4–8 mg IV.
High-Yield Pearls
In ICH, reversal is time-critical; every minute of ongoing coagulopathy can mean more hematoma expansion.
A focal deficit with vomiting and severe hypertension should keep hemorrhage high until CT proves otherwise.
Blood pressure reduction is helpful only if done smoothly; abrupt drops can worsen perfusion.
The Mimics
Ischemic stroke — CT distinguishes them; confusing them can lead to harmful thrombolysis.
Subarachnoid hemorrhage — thunderclap headache and cisternal blood dominate; missing ICH shifts you away from hematoma-expansion management.
Brain abscess/tumor — usually slower evolution; missing hemorrhage delays reversal and BP control.
Hypertensive encephalopathy — diffuse symptoms without focal CT bleed; confusing it with ICH may under-triage a surgical bleed.
Board Question
A 76-year-old man on warfarin presents with acute left-sided weakness and vomiting. CT shows a right basal ganglia hemorrhage. What is the best immediate reversal strategy?
AAspirin and clopidogrel
BAlteplase
C4-factor PCC plus IV vitamin K
DNo reversal is needed unless the INR is >5
Reveal answer
Correct: C
4-factor PCC plus IV vitamin K. Warfarin-associated intracerebral hemorrhage requires rapid factor replacement with PCC and durable reversal with vitamin K, ideally as soon as the bleed is identified. Waiting for a very high INR or giving antiplatelets would worsen bleeding.
Core ED reference for spontaneous ICH management: rapid CT diagnosis, severity scoring, blood pressure lowering, anticoagulant reversal, neurosurgical consultation, and disposition to stroke/neurocritical care.
4 of 4
Ankle Fractures / Ankle Dislocations
Ankle fractures and dislocations can hide skin tenting, vascular compromise, and compartment risk. A missed dislocation or unstable fracture can turn a...
A 28-year-old woman is sitting on the curb outside triage, white-faced and breathing through clenched teeth, one sneaker half-off and the other foot turned awkwardly beneath her. The ankle is swollen fast, shiny and angry-looking, and she keeps asking whether the bone is “sticking out” because she can’t bear to look. She heard and felt a sharp pop when she landed from a step-down box at the gym, then the foot twisted in a way that made everyone nearby wince. The pulses are still present, but the deformity is enough to make the room stop and look at you.
Before You Read
Which ankle injuries need immediate reduction before imaging?
What is the bedside exam that cannot be skipped before and after manipulation?
What findings make this a surgical, not outpatient, problem?
Why It Matters
Ankle fractures and dislocations can hide skin tenting, vascular compromise, and compartment risk. A missed dislocation or unstable fracture can turn a salvageable limb into a chronic disability.
When to Think of It
Visible deformity, gross instability, inability to bear weight, open wound, skin tenting, neurovascular symptoms, high-energy mechanism, or severe pain/swelling out of proportion. Dislocations and fracture-dislocations are emergencies; subtle fractures still need the right classification and follow-up.
Sick or Not Sick
The fork is “reduced/stable with intact skin and perfusion” versus “dislocated, open, tented, or neurovascularly threatened.” Any threatened skin or compromised pulses means reduction now, before the X-ray if the deformity is obvious.
The First Fifteen Minutes
Severe pain → fentanyl 25–50 mcg IV q5–10 min PRN or hydromorphone 0.5–1 mg IV q10–15 min PRN because analgesia improves cooperation for reduction.
Reduction of dislocated ankle/fracture-dislocation → procedural sedation per institutional protocol (e.g., ketamine or propofol-based RSI/sedation approach depending on physiology), because restoring alignment relieves skin and neurovascular threat.
Open fracture → cefazolin 2 g IV now (or 3 g IV if >120 kg; add gentamicin 5 mg/kg IV for heavily contaminated high-grade open injuries per local protocol), because early antibiotics reduce infection.
Tetanus prophylaxis if not up to date, because open wounds can seed tetanus.
If severe swelling/compartment concern → loose splinting and urgent ortho consult because constriction worsens ischemia.
Definitive Care & Disposition
Obtain plain radiographs after initial neurovascular assessment and after reduction if the joint was obviously dislocated. Unstable fracture patterns, open fractures, talar shifts, posterior malleolus involvement, syndesmotic injury, and any post-reduction incongruity generally need orthopedic involvement and often admission or urgent outpatient surgery planning. Stable isolated fractures can go in a splint/boot with non-weight-bearing instructions, crutches, analgesia, and close follow-up. Always document pre- and post-reduction pulses, cap refill, motor, and sensory exam.
How This One Kills
The failure mode is reducing the visible deformity but forgetting the pre/post neurovascular exam or missing an open injury under swelling—then the patient loses a limb or function overnight.
The Atypical Presentation
Older adults, intoxicated patients, and those with neuropathy may have surprisingly little pain despite major injury. Pediatric injuries can involve growth plates and look like “just a sprain,” with refusal to bear weight as the main clue. If swelling, ecchymosis, and function are out of proportion to the exam, image generously and keep the splint on until the story matches the films.
Back to Our Patient
Back to our 28-year-old with the obvious twisted ankle after landing from the box jump: this is an ankle fracture-dislocation until proven otherwise. Her foot needs an immediate pre-reduction neurovascular check, prompt reduction if deformity threatens skin or perfusion, then post-reduction exam and radiographs. If the wound is open or the reduction is unstable, ortho is involved early and antibiotics are started immediately. Once alignment and perfusion are restored, she can be splinted, kept non-weight-bearing, and dispositioned based on stability and follow-up needs.
Patient Presentation to Attending
“28-year-old woman with a twisting injury landing from a box jump, now with marked ankle deformity, rapid swelling, and severe pain, but intact pulses on arrival. I’m concerned for ankle fracture-dislocation; I’ve already done a neurovascular exam and the skin is starting to tent medially. I’m giving IV analgesia and preparing for urgent reduction with sedation before imaging if needed to protect the skin and perfusion. After reduction I’ll repeat the neurovascular exam, obtain X-rays, and involve orthopedics depending on stability and fracture pattern.”
Study Directive
Rehearse the pre/post reduction neurovascular checklist from memory.
Review Ottawa ankle rules and know when they do not apply well.
Practice a reduction-sedation plan and drug doses for a gross ankle dislocation.
Look at radiographs of bimalleolar, trimalleolar, and fracture-dislocation patterns and name which are unstable.
Key Medications
Fentanyl: 25–50 mcg IV q5–10 min PRN.
Hydromorphone: 0.5–1 mg IV q10–15 min PRN.
Ketamine for procedural sedation: 1–2 mg/kg IV or 4–5 mg/kg IM; dose varies with sedation depth and protocol.
Propofol for procedural sedation: 0.5–1 mg/kg IV bolus, then titrate; hypotension risk.
Cefazolin: 2 g IV once; 3 g if >120 kg.
Gentamicin: 5 mg/kg IV once for selected contaminated high-grade open fractures; check protocol/renal function.
Tetanus vaccine ± TIG: per immunization history and wound type; follow protocol.
High-Yield Pearls
A palpable pulse does not exclude a limb-threatening dislocation; skin tension and perfusion still matter.
Always document neurovascular status before and after reduction, not just after.
If the injury looks “just like a sprain” but the patient cannot bear weight or the swelling is explosive, think fracture until proven otherwise.
The Mimics
Ankle sprain — ligaments hurt, but true inability to bear weight, deformity, or bony tenderness over the malleoli suggests fracture/dislocation; confusing them under-treats unstable injuries.
Foot fracture (e.g., Lisfranc) — midfoot pain and plantar ecchymosis are the clues; missing it leads to chronic collapse.
Achilles tendon rupture — inability to plantarflex and positive Thompson test, not ankle deformity; confusing it with fracture delays repair decisions.
Tibia/fibula shaft injury — pain and deformity may extend above the ankle; missing proximal injury can overlook a more unstable pattern.
Board Question
A 24-year-old man presents with a visibly deformed ankle after a basketball injury. The foot is pale but still has a palpable dorsalis pedis pulse. What is the next best step?
AObtain ankle radiographs before any intervention
BImmediate reduction of the ankle dislocation
CDischarge with a walking boot
DApply ice and reassess in 2 hours
Reveal answer
Correct: B
Immediate reduction of the ankle dislocation. Gross deformity with threatened skin or vascular compromise requires urgent reduction before imaging because realignment restores perfusion and protects soft tissues. Radiographs can follow once the limb is stabilized.
A practical pediatric reference for distinguishing physeal and transitional ankle fractures and knowing which injuries need reduction, immobilization, and urgent orthopedic follow-up.
This trial informs ED disposition and counseling for isolated unstable lateral malleolus fractures by testing whether cast immobilization can be a safe alternative to routine operative fixation in selected patients.
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
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. What’s the diagnosis, and the first move?
Check your answer
Polymorphic VT. 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.
From the June 23 edition
Today, three days ago: Succinylcholine. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
1.5 mg/kg IV once for RSI. IM rescue dose: 4 mg/kg IM when IV access unavailable in cannot-control scenario per protocol. Known/suspected hyperkalemia, major burns/crush/denervation after risk window, neuromuscular disease, malignant hyperthermia history, pseudocholinesterase deficiency, penetrating eye injury caution.
From the June 16 edition
An 86-year-old woman on apixaban falls from standing, is awake, and has a small scalp laceration. She is normotensive but mildly tachypneic and “seems off” to her daughter. Which is the best next step?
ADischarge if CT head is negative
BReassure because the fall was low energy
CTreat as higher-risk trauma with imaging and anticoagulant-focused evaluation
DGive naloxone and observe
Reveal answer
Correct · C
Older adults on anticoagulants can have clinically important intracranial or occult injury after ground-level falls despite normal blood pressure. Low-energy mechanism does not equal low risk; imaging and careful reassessment are the safe path.
Journal Watch
From the FOAMed wireExtended window
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Chris Nickson and Lloyd Roberts VAFI and FARSI VAFI is video-assisted flexible intubation and FARSI is flexiscope-assisted rapid sequence intubation. These hybrid airway techniques are used to overcome supraglottic and infraglottic airway problems, respectively.
ABEM President Dr. James Thomas discusses updates to the new certifying exam, MyEMCert modules, declining qualifying exam pass rates, and new emergency department subspecialties. The post A Conversation With ABEM President James D. Thomas, MD 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...
This month Mike and Sanjay cover 20 papers, then Ultra Summarized by Jenny and Jess. Ken and Swami give us a lecture on why relative risk must always be paired with absolute risk and NNT to determine whether a...
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
Atropine dries secretions; pralidoxime treats nicotinic weakness. A patient can be dry and still die from respiratory muscle failure without 2-PAM.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Toxicology
Sodium Channel Blocker Toxicity
A wide QRS with a terminal R wave in aVR after overdose is sodium-channel blockade until proven otherwise.
The Tracing
A 29-year-old patient is brought in somnolent after an unknown ingestion. The ECG shows sinus tachycardia with a QRS of 142 ms, a tall terminal R wave in aVR, and a slurred S wave in lead I. Blood pressure is soft and the patient has intermittent ventricular ectopy. The pill bottle history is unclear.
QRS widening, often >100 ms and especially concerning when >120–160 ms
Terminal R wave in aVR or R/S ratio >0.7 in aVR
Rightward terminal QRS axis with deep terminal S wave in lead I
Sinus tachycardia is common with anticholinergic co-toxicity, especially TCAs
Severe cases can progress to ventricular dysrhythmias, hypotension, seizures, or Brugada-like patterns
Pearls
The ECG is the antidote trigger. Sodium bicarbonate is indicated for QRS widening, ventricular dysrhythmia, or hypotension from sodium-channel blockade.
TCAs are classic, but the pattern also appears with carbamazepine, diphenhydramine, cocaine, certain antipsychotics, and other sodium-channel blockers.
The treatment target is QRS narrowing and hemodynamic improvement, not a specific blood pH number in isolation.
Pitfalls
Do not anchor on the stated ingestion; patients often do not know or do not tell you what they took.
A normal early ECG can evolve. Repeat ECGs are part of the tox workup when the history is concerning.
Amiodarone can worsen sodium-channel blockade physiology; discuss with poison control for ventricular dysrhythmias.
At the Bedside
Give sodium bicarbonate boluses for QRS widening, hypotension, or ventricular dysrhythmia; repeat until QRS narrows and perfusion improves. Treat seizures aggressively, call poison control, and prepare vasopressors or lipid therapy for refractory shock depending on agent.
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 · Aneurysmal Subarachnoid Hemorrhage
Self-Examination
Test Your Understanding
A 52-year-old woman presents with sudden maximal-intensity headache, vomiting, and neck stiffness. Noncontrast head CT shows blood in the basal cisterns. Which additional therapy most reduces the risk of delayed ischemic neurologic deficits?
AMannitol
BNimodipine
CDexamethasone
DPhenytoin prophylaxis
Reveal answer
Correct answer · B
Nimodipine. Nimodipine is given to patients with aneurysmal SAH because it reduces delayed ischemic deficits, likely through neuroprotective and vasospasm-related effects. Mannitol may be used for ICP crises, steroids do not help, and routine anticonvulsant prophylaxis is not the key disease-modifying therapy.