An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
METATARSAL FRACTURES AND DISLOCATIONS
Missed Lisfranc and displaced metatarsal injuries lead to chronic midfoot instability, post-traumatic arthritis, deformity, and disability. The key emergency decision is whether alignment and perfusion can safely wait for definitive orthopedic care.
Also known asmetatarsal fracture · Lisfranc injury · tarsometatarsal dislocation · Jones fracture
A 27-year-old man arrives with a muddy sneaker half-laced and a rapidly swelling midfoot after his motorcycle tipped at low speed. He says the foot “folded” when he planted it, and the plantar surface is beginning to discolor beneath the arch. His toes are warm, but he cannot bear weight and winces when the forefoot is gently compressed. The radiographs are not yet in the room, and the decision about whether this foot can wait remains unresolved.
— What’s your move? Read on.
Before you read
How do you recognize a Lisfranc injury when plain films are subtle?
Which fractures require reduction, operative fixation, or prolonged non-weight-bearing?
When to Think of It
Suspect injury after axial loading, plantarflexion, crush, twisting, or a fall onto the forefoot. Look for plantar ecchymosis, midfoot swelling, inability to bear weight, focal metatarsal tenderness, shortening/rotation of a toe, or a widened gap between the first and second metatarsals. A “sprain” with disproportionate midfoot pain is Lisfranc until excluded.
Sick or Not Sick
Sick vs. not sick is primarily threatened neurovascular status or irreducible/open deformity vs. stable, closed injury. The call that matters most: does the foot require immediate reduction and orthopedic intervention, rather than routine splinting and follow-up?
The First Fifteen Minutes
Expose the entire foot; document dorsalis pedis/posterior tibial pulses, capillary refill, temperature, sensation, and toe movement before and after immobilization.
Obtain AP, lateral, and oblique foot radiographs; add weight-bearing views only if safe and tolerated. Obtain CT for suspected Lisfranc injury or complex fracture when radiographs are nondiagnostic.
For significant pain: fentanyl 50–100 micrograms IV/IN, repeat 25–50 micrograms every 5 minutes IV as needed, because μ-opioid analgesia rapidly blunts severe nociceptive pain. Monitor ventilation.
For a cooperative patient needing manipulation: ketamine 1 mg/kg IV, repeat 0.25–0.5 mg/kg as needed, because dissociative analgesia preserves spontaneous ventilation and facilitates reduction. Dose varies by local sedation protocol; check institutional guidance. Alternatively, propofol 0.5–1 mg/kg IV, followed by 0.25–0.5 mg/kg increments, provides rapid sedation but can cause apnea and hypotension; use only with airway-capable monitoring.
Open wound or gross contamination: give cefazolin 2 g IV (3 g if ≥120 kg) promptly, because early gram-positive coverage reduces infection risk; add broader coverage for farm, water, or heavily contaminated wounds per protocol.
If deformity, skin tenting, absent pulse, or progressive neurologic deficit is present: urgent reduction under analgesia/sedation, then repeat and document neurovascular examination. Do not delay reduction for advanced imaging.
Tetanus prophylaxis: Tdap or Td 0.5 mL IM if indicated; for dirty wounds with unknown/incomplete vaccination, add tetanus immune globulin 250 units IM, because passive antitoxin bridges inadequate immunization.
Definitive Care & Disposition
Apply a well-padded posterior splint, often with a stirrup component, and keep the foot elevated. Nondisplaced, stable fractures may receive protected or non-weight-bearing immobilization with orthopedic follow-up. Displaced, angulated, rotated, multiple, open, intra-articular, or Lisfranc injuries need urgent orthopedic consultation; unstable Lisfranc injuries generally require operative fixation after swelling permits, while open injuries require irrigation/debridement and antibiotics. Admit if reduction is unstable, perfusion is threatened, the injury is open, swelling is severe, pain is uncontrolled, or social circumstances make non-weight-bearing unsafe.
How This One Kills
The dangerous miss is a subtle Lisfranc disruption diagnosed as a midfoot sprain, followed by weight-bearing; displacement and ligament failure produce chronic arch collapse and post-traumatic arthritis.
The Differential — What Else Looks Like This
Lisfranc ligament injury — plantar ecchymosis or first–second metatarsal malalignment; confusing it with an isolated metatarsal fracture causes missed instability.
Compartment syndrome — escalating pain with passive toe stretch and tense compartments; confusing it with ordinary swelling delays fasciotomy.
Turf toe/plantar plate injury — plantar first-MTP tenderness without fracture alignment abnormality; confusing it with a displaced fracture leads to incorrect immobilization or missed soft-tissue injury.
Sesamoid fracture — focal plantar first-MTP pain; confusing it with a metatarsal shaft injury misdirects imaging and weight-bearing advice.
The Second-Day Story
Older adults, patients with neuropathy, and partially treated injuries may have little pain or no memorable trauma. A diabetic patient may present only with swelling, warmth, or inability to walk. Compare both feet, inspect the plantar surface, obtain weight-bearing imaging when safe, and maintain a low threshold for CT when the mechanism and examination disagree with plain films.
Back to Our Patient
Back to the 27-year-old man with the muddy sneaker and plantar ecchymosis: the trigger presentation is axial-loading midfoot trauma with inability to bear weight, so Lisfranc injury and metatarsal fracture must be assumed until excluded. His pulses and toe sensation are intact, making him currently stable, but the plantar bruising makes the injury high risk rather than a routine sprain. He receives IV fentanyl, foot radiographs followed by CT showing tarsometatarsal malalignment, and a well-padded non-weight-bearing splint; because the injury is unstable, orthopedics admits him for operative planning.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 27-year-old man with high-risk midfoot trauma after his motorcycle tipped while his planted foot twisted, now with severe swelling, inability to bear weight, and plantar ecchymosis. He has no open wound, but has marked tarsometatarsal tenderness and pain with forefoot stress; dorsalis pedis and posterior tibial pulses, capillary refill, sensation, and toe movement are intact. There is no compartment firmness or pain out of proportion at this time. Initial foot films are concerning for first–second metatarsal malalignment, and CT confirms an unstable Lisfranc injury. I gave IV fentanyl, immobilized him without weight-bearing, and consulted orthopedics for admission and operative management.”
Study Directive
Draw the Lisfranc joint complex and label the “fleck sign.” Review three foot radiograph sets and identify metatarsal alignment, displacement, and open injury features. Practice a complete pre- and post-reduction neurovascular exam, then state admission criteria from memory.
Poutoglidou F, van Groningen B, McMenemy L, et al. · Bone Joint J, 2024 · PMID 39615511 · cited 10×
Provides a current framework for recognizing acute Lisfranc instability, choosing appropriate imaging, and arranging timely operative referral to prevent chronic midfoot pain and deformity.
More in Today's Issue
7 additional topics
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TALUS INJURIES
Talar fractures and peritalar dislocations can compromise skin, blood flow, and the talar blood supply. Delay in reduction increases soft-tissue injury and...
Also known astalar fracture · talar neck fracture · talar body fracture · osteochondral lesion of the talus
A 34-year-old climber lies on the trauma stretcher with his boot cut away and his ankle locked at an unnatural angle. His foot is cool compared with the opposite side, and the skin blanches over the dorsum where bone is pressing from beneath. He remembers landing hard with the foot trapped, but cannot describe the position of the ankle. The pulses are difficult to find, and the next move has not yet been made.
Before You Read
Which talar injury demands immediate reduction?
Why is the talar neck fracture uniquely vulnerable to avascular necrosis?
What imaging is needed after the ankle appears “back in place”?
Why It Matters
Talar fractures and peritalar dislocations can compromise skin, blood flow, and the talar blood supply. Delay in reduction increases soft-tissue injury and risks permanent osteonecrosis, malunion, and arthritis.
When to Think of It
Suspect talus injury after high-energy axial loading, forced dorsiflexion, or an ankle/foot deformity. Look for an irreducible or dislocated ankle, lateral or medial displacement of the foot, inability to bear weight, swelling, skin tenting, and neurovascular changes. A talar neck fracture may be subtle on initial radiographs despite major downstream consequences.
Sick or Not Sick
The decisive fork is deformed or threatened neurovascular foot vs. closed, aligned, perfused injury. Any open injury, skin tenting, dislocation, or ischemia requires immediate reduction and orthopedic involvement.
The First Fifteen Minutes
Remove constrictive footwear, cover open wounds, document pulses, sensation, and motor function, and obtain AP/lateral/mortise ankle plus foot radiographs if this does not delay reduction.
For severe pain: fentanyl 50–100 micrograms IV/IN, repeat 25–50 micrograms IV every 5 minutes as needed, because it rapidly reduces pain during preparation for reduction.
For urgent reduction: ketamine 1 mg/kg IV, repeat 0.25–0.5 mg/kg as needed, because dissociation provides analgesia and muscle relaxation while generally preserving spontaneous breathing. Follow local procedural-sedation policy.
If ketamine is unsuitable: propofol 0.5–1 mg/kg IV, then 0.25–0.5 mg/kg increments, because it produces rapid sedation; anticipate apnea and hypotension.
If open: cefazolin 2 g IV (3 g if ≥120 kg) immediately, because early antibiotic coverage decreases deep infection risk; add gram-negative/anaerobic coverage for severe contamination according to protocol.
For an open contaminated wound with inadequate immunization: Tdap/Td 0.5 mL IM; add tetanus immune globulin 250 units IM when vaccination is unknown or incomplete.
Reduce promptly, then repeat pulses, capillary refill, sensation, and motor examination. Apply a well-padded posterior splint and elevate.
Definitive Care & Disposition
All displaced talar neck/body fractures, talar dislocations, open injuries, and unstable osteochondral injuries require urgent orthopedic consultation and usually admission. CT after reduction defines fracture pattern and operative planning. Definitive treatment ranges from strict non-weight-bearing for selected nondisplaced fractures to open reduction and internal fixation; open injuries require operative irrigation/debridement. Monitor for compartment syndrome, infection, malunion, post-traumatic arthritis, and avascular necrosis during prolonged follow-up.
How This One Kills
The lethal orthopedic error is leaving a talar or peritalar dislocation unreduced while obtaining “better imaging,” allowing skin necrosis and further disruption of the talus’ tenuous blood supply.
The Atypical Presentation
A nondisplaced talar neck fracture may present as an ordinary ankle sprain with mild swelling and preserved pulses. In an older patient or a patient with neuropathy, pain may be unimpressive. Mechanism, focal deep ankle tenderness, inability to bear weight, and persistent pain despite “normal” ankle films should prompt CT and orthopedic follow-up.
Back to Our Patient
Back to the 34-year-old climber with the cool, deformed foot: this is an immediately threatened talar/peritalar injury, not a routine ankle fracture. He receives IV fentanyl and ketamine-assisted urgent reduction, after which pulses and warmth return; repeat films show a reduced joint with suspected talar neck fracture. He is placed in a padded splint, remains strictly non-weight-bearing, receives cefazolin because of a small open wound, and is admitted to orthopedics for CT and operative planning.
Patient Presentation to Attending
“This is a 34-year-old climber with a high-energy forced-landing injury and a grossly deformed, initially cool ankle with skin tenting. Before reduction, pulses were difficult to detect, but motor and sensation were present; there is a small dorsal wound and no evidence yet of compartment syndrome. I gave fentanyl and performed ketamine-assisted urgent reduction, with return of palpable pulses and improved warmth. Post-reduction films show an aligned ankle with a suspected talar neck fracture. He received cefazolin and tetanus assessment, is splinted and non-weight-bearing, and needs admission for CT and urgent orthopedic management.”
Study Directive
Memorize the Hawkins talar neck classification and its avascular-necrosis risk gradient. Practice verbalizing the reduction trigger and post-reduction exam. Review three CT cases and identify talar neck, body, lateral-process, and osteochondral injuries.
Key Medications
Fentanyl: 50–100 micrograms IV/IN, then 25–50 micrograms IV every 5 minutes as needed.
Ketamine: 1 mg/kg IV, repeat 0.25–0.5 mg/kg; pediatric dosing and sedation monitoring differ—follow institutional protocol.
Propofol: 0.5–1 mg/kg IV, then 0.25–0.5 mg/kg increments; check a procedural-sedation reference if uncertain.
Cefazolin: 2 g IV, or 3 g IV if ≥120 kg; broaden for contaminated wounds according to local protocol.
Tdap/Td: 0.5 mL IM; tetanus immune globulin 250 units IM when indicated.
High-Yield Pearls
A “normal” pulse does not make a displaced talus injury safe; skin and talar blood supply remain at risk.
Hawkins sign on follow-up radiographs suggests preserved talar vascularity; its absence raises concern for osteonecrosis but is not an acute ED finding.
Reduce first, then obtain CT—unless the foot is already aligned and stable.
The Mimics
Ankle dislocation without fracture — joint alignment and CT distinguish it; confusing the two underestimates operative fracture complexity.
Calcaneus fracture — heel widening and axial-load mechanism; confusing it with talus injury misses different imaging and fixation needs.
Tibial plafond fracture — distal tibial articular injury on CT; confusing it with talar injury misjudges prognosis and reduction strategy.
Acute compartment syndrome — tense compartments and escalating pain; confusing it with expected swelling delays fasciotomy.
Board Question
A patient has a displaced talar neck fracture with dislocation and absent distal pulses. What is the immediate priority?
AMRI to evaluate avascular necrosis
BOutpatient CT within 48 hours
CUrgent reduction with repeated neurovascular examination
DWeight-bearing radiographs
Reveal answer
Correct: C
Dislocation and vascular compromise require immediate reduction; imaging must not delay restoration of alignment and perfusion. CT follows reduction for fracture characterization.
A current overview of talus fracture management, including recognition, imaging, initial stabilization, and operative indications for these high-risk injuries.
Multicenter outcome data clarify how surgical approach and fixation affect complications, helping inform early orthopedic consultation and counseling about avascular necrosis and other risks.
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CENTRAL RETINAL ARTERY OCCLUSION
Central retinal artery occlusion is an ocular ischemic stroke with a narrow window for possible reperfusion and a substantial risk of concurrent cerebral or...
Also known asCRAO · retinal artery occlusion · eye stroke
A 68-year-old woman notices that the right half of the newspaper has vanished while drinking coffee; the cup slips from her hand as she tries to focus. She reports sudden, painless monocular darkness beginning 70 minutes ago and keeps covering one eye, then the other, hoping the image will return. Her temporal scalp feels tender, though she calls it “just a headache.” The emergency team has not yet decided whether the clock is still actionable.
Before You Read
What makes sudden monocular vision loss a stroke emergency?
Which history changes treatment immediately by suggesting giant cell arteritis?
What should happen even when ocular reperfusion therapies are uncertain?
Why It Matters
Central retinal artery occlusion is an ocular ischemic stroke with a narrow window for possible reperfusion and a substantial risk of concurrent cerebral or carotid disease. Missing giant cell arteritis can blind the second eye and cause systemic ischemic catastrophe.
When to Think of It
Sudden, painless, profound monocular vision loss with a relative afferent pupillary defect is the trigger. Fundoscopy may show retinal whitening with a cherry-red spot, but early examination can be subtle. Ask about transient preceding episodes, jaw claudication, new headache, scalp tenderness, polymyalgia symptoms, vascular risk factors, atrial fibrillation, neck trauma, and dissection symptoms.
Sick or Not Sick
The key call is true acute retinal ischemia within a potentially treatable window, or arteritic CRAO requiring immediate steroids, versus a non-CRAO mimic. Treat as stroke until proven otherwise; do not let a normal neurologic examination lower urgency.
The First Fifteen Minutes
Activate stroke/ophthalmology pathways; record exact last-known-well time, visual acuity, pupils, fields, ocular motility, and fundus findings.
Obtain glucose, CBC/platelets, CMP, PT/INR, aPTT, ECG, and urgent brain/vascular imaging—typically noncontrast head CT plus CTA head/neck—to evaluate hemorrhage, carotid disease, dissection, and concurrent cerebral ischemia.
If giant cell arteritis is suspected, draw ESR, CRP, and platelets but do not delay treatment: methylprednisolone 500–1,000 mg IV daily for threatened bilateral/severe visual loss, because rapid glucocorticoid therapy suppresses arteritic ischemia; dosing varies by ophthalmology/rheumatology protocol, so check an institutional reference.
If non-arteritic CRAO is suspected and hemorrhage is excluded, give aspirin 325 mg PO once, then 81 mg daily when appropriate, because it reduces recurrent vascular events even though it does not reliably restore retinal flow.
In a highly selected patient within 4.5 hours, without contraindications, discuss alteplase 0.9 mg/kg IV, maximum 90 mg: 10% as a bolus and the remainder over 60 minutes with stroke and ophthalmology teams. This is protocol-dependent and controversial for CRAO; check current institutional eligibility criteria rather than treating routinely.
Do not delay transfer for ocular massage or anterior-chamber paracentesis; benefit is unproven and potential harm exists. If ophthalmology recommends an IOP-lowering trial, acetazolamide 500 mg IV once may be used, because reducing intraocular pressure can improve perfusion pressure; check renal function, electrolytes, and sulfonamide-related contraindications.
Definitive Care & Disposition
Admit or transfer urgently to a stroke-capable center with ophthalmology and neurology involvement. Evaluate for carotid stenosis/dissection, atrial fibrillation, and vascular risk factors; arrange echocardiography and rhythm monitoring when indicated. Carotid endarterectomy may be needed for symptomatic high-grade carotid stenosis. All CRAO patients require secondary prevention and close ophthalmologic follow-up; suspected GCA requires biopsy or ultrasound-guided confirmation while steroids continue.
How This One Kills
The catastrophic miss is labeling the event “just an eye problem,” failing to evaluate carotid/cerebral ischemia, and missing GCA until the fellow eye is permanently blind.
The Atypical Presentation
Older adults may describe “blur,” missing letters, or a gray patch rather than blindness. A patient with prior cataract disease may attribute the change to the lens, and a partially recanalized artery may leave only a field defect. Test each eye separately, check for an afferent pupillary defect, and ask specifically about GCA symptoms even when the headache is mild or absent.
Back to Our Patient
Back to the 68-year-old woman with 70 minutes of painless monocular darkness and scalp tenderness: she has sudden retinal ischemia with a possible arteritic signal, so she is treated as a stroke emergency while GCA is investigated. Her right afferent pupillary defect and pale retina support CRAO; glucose is normal, CTA shows no hemorrhage but reveals severe ipsilateral carotid stenosis, and ESR/CRP are elevated. She receives immediate IV methylprednisolone, aspirin after hemorrhage exclusion, and urgent stroke/ophthalmology consultation; she is admitted for vascular management, with carotid intervention and long-term secondary prevention planned.
Patient Presentation to Attending
“This is a 68-year-old woman with 70 minutes of sudden, painless right monocular vision loss, associated with new scalp tenderness but no weakness, aphasia, or eye-movement pain. Visual acuity is profoundly reduced in the right eye with a right afferent pupillary defect, and fundoscopy shows retinal whitening with a cherry-red spot. Glucose is normal, and CTA shows severe right carotid stenosis without intracranial hemorrhage. I am concerned for central retinal artery occlusion, with giant cell arteritis still possible. I sent ESR, CRP, and platelets, gave IV methylprednisolone and aspirin after imaging, and am arranging emergent stroke and ophthalmology admission for reperfusion consideration and carotid management.”
Study Directive
Practice a one-minute monocular vision-loss history distinguishing CRAO, CRVO, retinal detachment, and optic neuritis. Memorize the alteplase dose and contraindication framework, then review your local CRAO transfer protocol. Draw the carotid-to-retina embolic pathway and list five causes of embolism.
Key Medications
Methylprednisolone: 500–1,000 mg IV daily for severe visual-threat GCA; dose varies—check ophthalmology/rheumatology protocol. Pediatric therapy is specialist-directed.
Aspirin: 325 mg PO once, then commonly 81 mg PO daily when indicated; avoid if bleeding or allergy.
Alteplase: 0.9 mg/kg IV, maximum 90 mg; 10% bolus and remainder over 60 minutes. CRAO use is controversial and requires stroke-protocol confirmation.
Acetazolamide: 500 mg IV once for selected ophthalmology-directed IOP reduction; check renal function and electrolytes.
High-Yield Pearls
A normal neurologic examination does not make CRAO nonurgent; the retina is brain tissue.
New headache, jaw claudication, or scalp tenderness changes the first medication from “vascular prevention” to immediate high-dose steroids.
CRAO treatment evidence is limited, but vascular-source evaluation and secondary prevention are not optional.
The Mimics
Retinal detachment — flashes, floaters, and a curtain-like field loss rather than sudden profound arterial ischemia; confusing them delays stroke/GCA evaluation.
Amaurosis fugax — transient loss with full recovery; it still signals embolic disease but differs from persistent infarction.
Optic neuritis — painful eye movement and color desaturation, usually subacute; confusing it with CRAO triggers the wrong vascular workup.
Central retinal vein occlusion — generally subacute painless blurring with diffuse retinal hemorrhages; confusing it with CRAO misdirects reperfusion urgency.
Board Question
A 72-year-old has sudden painless monocular vision loss, jaw claudication, and an elevated ESR. What is the next best step?
AWait for temporal artery biopsy before treatment
BStart high-dose glucocorticoids immediately
CGive topical antibiotics
DReassure and arrange routine ophthalmology follow-up
Reveal answer
Correct: B
Suspected GCA with visual symptoms requires immediate high-dose glucocorticoids; biopsy or vascular ultrasound should not delay treatment. The goal is preventing irreversible fellow-eye and systemic ischemia.
Treat CRAO as an acute ischemic stroke: activate emergent ophthalmologic and stroke evaluation, consider time-sensitive reperfusion, and initiate urgent vascular risk assessment and secondary prevention.
Individual-patient data suggest that earlier thrombolysis is associated with better visual outcomes, reinforcing rapid recognition and immediate referral to a thrombolysis-capable stroke center.
CRVO is usually not a thrombolysis emergency, but it can cause macular edema, retinal neovascularization, vitreous hemorrhage, and painful neovascular...
Also known asCRVO · retinal vein occlusion · eye stroke
A 63-year-old man reports that the vision in his left eye has become a red-gray blur over two days. He can still see shapes, but straight lines bend and the eye feels heavy rather than painful. His blood pressure cuff reads 218/116 in triage, and he says he stopped taking his medication months ago because he “felt fine.” The fundus examination is about to determine whether this is an isolated retinal problem or a sign of immediate systemic danger.
Before You Read
How does CRVO differ clinically from CRAO?
Which finding makes CRVO ischemic and high risk?
What emergency conditions must be excluded before outpatient retinal treatment?
Why It Matters
CRVO is usually not a thrombolysis emergency, but it can cause macular edema, retinal neovascularization, vitreous hemorrhage, and painful neovascular glaucoma. The ED must identify ischemic disease, severe hypertension, hyperviscosity, and mimics while arranging rapid retinal follow-up.
When to Think of It
Typical presentation is painless, unilateral, subacute visual blurring or field loss. Fundoscopy shows diffuse retinal hemorrhages, dilated tortuous veins, cotton-wool spots, and optic-disc edema—the “blood-and-thunder” retina. Risk factors include hypertension, diabetes, glaucoma, hyperlipidemia, thrombophilia, and hematologic disease.
Sick or Not Sick
The key call is ischemic CRVO, severe hypertension, acute glaucoma, or another vision-threatening process vs. non-ischemic CRVO suitable for urgent outpatient retina care. Ischemic features include profound visual loss, marked afferent pupillary defect, extensive hemorrhage, and retinal nonperfusion.
The First Fifteen Minutes
Measure visual acuity in each eye, pupils, fields, intraocular pressure, and perform dilated fundus examination when safe; obtain ocular ultrasound if the view is obscured.
Check glucose, CBC, CMP, and blood pressure; add ESR/CRP when symptoms raise concern for GCA and serum protein electrophoresis/viscosity studies when hyperviscosity is plausible.
If BP is ≥180/120 with encephalopathy, heart failure, kidney injury, or other acute end-organ damage, use nicardipine 5 mg/h IV, increasing by 2.5 mg/h every 5–15 minutes to a maximum of 15 mg/h, because controlled afterload reduction limits ongoing vascular injury. Target gradual reduction, not normalization; check local hypertensive-emergency protocol.
If there is no acute end-organ injury, do not rapidly lower BP solely because of the retinal finding; restart or adjust chronic therapy with follow-up rather than reflex IV medication.
Do not give empiric thrombolysis, heparin, or antiplatelet therapy solely to reverse CRVO; no proven acute benefit and bleeding risk exists. Start aspirin only for a separate cardiovascular indication, commonly 81 mg PO daily, after individualized assessment.
If painful red eye, markedly elevated IOP, corneal edema, and nausea suggest neovascular or angle-closure glaucoma, urgently involve ophthalmology; acetazolamide 500 mg IV once may be used to lower aqueous production, with renal/electrolyte screening and ophthalmology direction.
Definitive Care & Disposition
Urgent retina follow-up—often within days, sooner for ischemic CRVO or severe visual loss—is needed for OCT, fluorescein angiography, and intravitreal anti-VEGF therapy. Common specialist-administered options include bevacizumab 1.25 mg intravitreal, ranibizumab 0.5 mg intravitreal, or aflibercept 2 mg intravitreal; dosing and agent selection require ophthalmology protocol. Panretinal photocoagulation is used for neovascularization. Admit when hypertensive emergency, acute glaucoma, severe systemic disease, inability to access rapid ophthalmology, or diagnostic uncertainty is present; otherwise discharge with expedited retina care and risk-factor management.
How This One Kills
The dangerous miss is treating CRVO as benign blurred vision while ischemic retina develops neovascular glaucoma—an intensely painful, pressure-elevated eye that can progress to irreversible blindness.
The Atypical Presentation
A patient may have only mild blur, especially with non-ischemic CRVO, or may present late after adapting to one-eye visual loss. Bilateral disease suggests systemic hypertension, hyperviscosity, or inflammatory disease. Check the other eye, blood pressure, and visual acuity objectively; a quiet, painless eye does not imply low risk.
Back to Our Patient
Back to the 63-year-old man with two days of red-gray blur and BP 218/116: his subacute painless loss and hemorrhagic fundus indicate CRVO rather than CRAO, but the blood pressure demands immediate assessment for end-organ injury. He has diffuse retinal hemorrhages, venous tortuosity, and macular edema without severe afferent pupillary defect or painful high-pressure eye; labs show no acute kidney or cardiac injury. Because this is severe asymptomatic hypertension rather than hypertensive emergency, he does not receive IV antihypertensive therapy in the ED; his chronic regimen is restarted with close follow-up, and retina clinic evaluates him within 24–48 hours for anti-VEGF treatment.
Patient Presentation to Attending
“This is a 63-year-old man with two days of painless progressive left-eye blurring and a triage blood pressure of 218/116. Visual acuity is reduced but he can count fingers, with no severe afferent pupillary defect, no painful red eye, and no neurologic deficits. Fundoscopy shows diffuse retinal hemorrhages, dilated tortuous veins, and macular edema, consistent with central retinal vein occlusion. He has no chest pain, dyspnea, encephalopathy, kidney injury, or ECG evidence of acute end-organ damage. I would avoid thrombolysis and rapid IV blood-pressure reduction, restart chronic therapy, and arrange urgent retina follow-up for OCT and anti-VEGF treatment.”
Study Directive
Compare fundus images of CRAO, CRVO, diabetic retinopathy, and retinal detachment. Memorize the ischemic-CRVO danger signs and the hypertensive-emergency medication threshold. Create a disposition algorithm distinguishing discharge with urgent retina care from admission for glaucoma, ischemia, or systemic end-organ injury.
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Key Medications
Nicardipine: 5 mg/h IV, increase by 2.5 mg/h every 5–15 minutes, maximum 15 mg/h; follow local hypertensive-emergency protocol.
Aspirin: 81 mg PO daily only for an independent cardiovascular indication; not a proven acute CRVO reversal therapy.
Acetazolamide: 500 mg IV once for ophthalmology-directed IOP lowering; check renal function/electrolytes.
Intravitreal specialist therapies: bevacizumab 1.25 mg, ranibizumab 0.5 mg, or aflibercept 2 mg per injection; dosing and repeated schedules vary—confirm with ophthalmology or institutional protocol. Pediatric retinal disease requires specialist dosing.
High-Yield Pearls
CRVO is usually subacute and hemorrhagic; CRAO is typically sudden and pale.
Do not rapidly lower blood pressure in asymptomatic severe hypertension without acute end-organ injury.
Ischemic CRVO is defined by retinal dysfunction and nonperfusion—not simply by the amount of visible hemorrhage.
The Mimics
CRAO — sudden profound loss with pale retina and cherry-red spot; confusing it with CRVO loses a stroke/GCA evaluation window.
Retinal detachment — curtain, flashes, or floaters with a detached membrane on ultrasound; confusing it delays surgical repair.
Diabetic retinopathy/vitreous hemorrhage — diabetes and poor fundus view may mimic CRVO; confusing them misses a different retinal treatment pathway.
Hypertensive retinopathy — bilateral arteriolar narrowing, hemorrhages, and cotton-wool spots with severe BP; confusing it with unilateral CRVO may obscure hypertensive emergency.
Board Question
Which finding most strongly suggests ischemic rather than non-ischemic CRVO?
AMild unilateral blur with preserved visual acuity
BProfound visual loss with a marked relative afferent pupillary defect
CIsolated increased intraocular pressure with a normal fundus
DFlashes and a peripheral retinal tear
Reveal answer
Correct: B
Profound visual loss and a marked afferent pupillary defect indicate extensive retinal ischemia and higher risk of neovascular complications. These patients need especially urgent ophthalmologic surveillance.
Evaluate suspected asymmetric optic nerve or severe retinal dysfunction.Assess unexplained unilateral or asymmetric vision loss.Establish a baseline...
Also known asRAPD · Marcus Gunn pupil
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Indications
Evaluate suspected asymmetric optic nerve or severe retinal dysfunction.
Assess unexplained unilateral or asymmetric vision loss.
Establish a baseline pupillary examination in neurologic, orbital, or ocular disease.
Contraindications
No absolute contraindication.
Defer or modify testing if the patient cannot fixate, has severe photophobia, altered mental status, or bilateral ocular trauma; document limitations.
Pharmacologic dilation, iris trauma, or marked anisocoria can make interpretation unreliable.
Equipment & Prep
Penlight or bright, focused examination light.
Dim room when possible; ask the patient to remove sunglasses and contact lenses if feasible.
Seat the patient comfortably and instruct them to fixate on a distant target.
Avoid shining the light directly at the target, which may provoke a near response.
Steps
Inspect pupil size, shape, symmetry, and reactivity in ambient light; note anisocoria before illumination.
Ask the patient to fixate on a distant target throughout the examination.
Illuminate one eye for approximately 2–3 seconds and observe the direct response; simultaneously observe the consensual response in the opposite eye.
Move the light briskly to the opposite eye, maintaining illumination for approximately 2–3 seconds.
Repeat the swing several times at a steady cadence, comparing the initial constriction and any subsequent redilation.
Identify the eye with the relative afferent defect: when light is moved to that eye, both pupils constrict less or dilate.
If quantification is needed, use neutral-density filters over the better eye, increasing density until the responses appear symmetric; document the approximate grade according to local convention.
Confirmation & Success Criteria
A reproducible relative dilation, or noticeably weaker constriction, when light is directed at the affected eye confirms an RAPD.
The finding is relative: an abnormal response may reflect optic nerve disease, severe asymmetric retinal disease, or profound asymmetric visual loss.
Record laterality and grade; absence of an RAPD does not exclude bilateral or symmetric disease.
If findings are inconsistent, repeat after optimizing fixation, room lighting, and stimulus intensity.
Complications & Rescue
The examination itself should not injure the eye.
False results may occur with poor fixation, unequal illumination, examiner fatigue, pharmacologic dilation, iris damage, or rapidly alternating light exposure.
If apparent anisocoria is mistaken for an RAPD, reassess pupil size before and after illumination and compare both direct and consensual responses.
If the patient cannot fixate, use a distant target, brief occlusion of the non-tested eye when appropriate, or document that the test is limited.
Aftercare & Documentation
No specific aftercare is required.
Document pupil size and shape, direct and consensual responses, fixation quality, laterality and grade of RAPD, visual acuity, and relevant ocular findings.
Escalate urgently for a new RAPD with acute vision loss, neurologic deficit, painful red eye, proptosis, or suspected orbital/optic nerve disease.
6 of 8 · Procedure Corner
Digital Ocular Massage
May be considered as a temporizing maneuver for suspected central retinal artery occlusion only after urgent ophthalmology consultation and while definitive...
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Indications
May be considered as a temporizing maneuver for suspected central retinal artery occlusion only after urgent ophthalmology consultation and while definitive evaluation or transfer is underway.
Do not allow massage to delay stroke-center evaluation, ocular therapy, or time-sensitive specialist-directed treatment.
Evidence for visual benefit is uncertain; routine use is not established.
Contraindications
Suspected open-globe injury, penetrating trauma, globe rupture, or recent ocular surgery unless specifically directed by the treating ophthalmologist.
Hyphema, severe ocular pain with a firm globe, obvious orbital trauma, or concern for retinal/choroidal injury.
Do not apply pressure directly to the cornea or an exposed ocular surface.
Equipment & Prep
Gloves, examination light, and visual-acuity and pupillary-assessment supplies.
Explain that the maneuver is temporary and unproven, and obtain consent when circumstances permit.
Exclude obvious trauma or open globe; document baseline vision, pupils, pain, and intraocular pressure if clinically appropriate.
Keep the patient monitored and coordinate immediate ophthalmology/stroke consultation.
Steps
Position the patient comfortably, with the head supported and the affected eye gently closed.
Place a clean fingertip over the closed upper eyelid, using only the broad padded finger surface; avoid the cornea, eyelid margin, and direct focal pressure.
Apply gentle, brief pressure for approximately 5–10 seconds, then release completely for a similar interval.
Repeat alternating pressure and release for several minutes only if directed by the consultant or local protocol; stop immediately for pain, bleeding, nausea, bradycardia, or worsening vision.
Reassess visual acuity if possible, pupils, pain, and ocular appearance while arranging definitive care.
Confirmation & Success Criteria
There is no reliable bedside endpoint proving retinal reperfusion.
Transient subjective improvement or a change in pupillary findings is not sufficient to establish efficacy.
Success is completion without ocular injury while urgent definitive evaluation and treatment proceed.
Persistent or worsening vision loss requires continued emergency management, regardless of the response to massage.
Complications & Rescue
Potential harms include increased intraocular pressure, corneal injury, hyphema, retinal or choroidal injury, pain, vagal symptoms, and delay of effective therapy.
Stop for pain, new bleeding, corneal abnormality, worsening vision, bradycardia, or patient intolerance.
Reassess the globe and obtain urgent ophthalmologic evaluation if injury is suspected.
If CRAO is suspected, treat it as an ocular and vascular emergency; do not substitute massage for stroke evaluation or specialist-directed reperfusion therapy.
7 of 8 · Supplemental — C3
Vision Loss
Localize acute vision loss to the ocular media, retina, optic nerve, retrochiasmal pathways, or cortex using a focused emergency examination.Recognize...
Also known asacute vision loss · sudden vision loss · amaurosis · amaurosis fugax · monocular vision loss
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Learning Objective
Localize acute vision loss to the ocular media, retina, optic nerve, retrochiasmal pathways, or cortex using a focused emergency examination.
Recognize time-critical patterns requiring immediate ophthalmology, neuro-ophthalmology, or stroke consultation.
Core Concepts
First establish onset, monocular versus binocular symptoms, persistent versus transient course, pain, field pattern, trauma, headache, vascular risks, and medication or toxin exposure.
Measure each eye separately: visual acuity, visual fields, pupils, color vision when feasible, ocular motility, and external/anterior-segment findings.
A relative afferent pupillary defect indicates asymmetric optic nerve or severe retinal dysfunction; it may be absent with bilateral or symmetric disease.
A monocular “curtain,” flashes/floaters, or field defect suggests retinal pathology; a painful red eye with reduced vision suggests corneal, uveal, or pressure-related disease.
Sudden painless monocular loss is an emergency differential that includes retinal artery occlusion, retinal detachment, vitreous hemorrhage, and ischemic optic neuropathy.
Binocular field loss localizes posterior to the chiasm; associated neurologic deficits or cortical symptoms require stroke evaluation.
Retrieval Prompt
A patient has sudden painless monocular vision loss and a relative afferent pupillary defect. What broad localization should be prioritized? → Severe asymmetric retinal dysfunction or optic nerve disease, including retinal artery occlusion and ischemic optic neuropathy.
8 of 8 · Supplemental — Imaging
US of Central Retinal Artery Occlusion
Use ocular ultrasound as an adjunct in acute vision loss to assess the globe, exclude major mimics, and evaluate retinal or optic-nerve-adjacent findings...
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Learning Objective
Use ocular ultrasound as an adjunct in acute vision loss to assess the globe, exclude major mimics, and evaluate retinal or optic-nerve-adjacent findings when the fundus view is limited.
Understand that a normal or nondiagnostic scan does not exclude central retinal artery occlusion and must not delay definitive evaluation.
Core Concepts
Perform a gentle closed-lid examination with copious gel; avoid pressure when open globe, ocular trauma, or globe rupture is possible.
Standard B-scan is best for detecting retinal detachment, vitreous hemorrhage, lens dislocation, and gross structural abnormalities; these findings do not directly diagnose CRAO.
Color or spectral Doppler may show reduced or absent central retinal artery flow, but vessel identification and flow assessment are technically difficult and operator-dependent.
CRAO is primarily a clinical and funduscopic diagnosis; ultrasound has limited sensitivity and cannot reliably distinguish all causes of acute retinal ischemia.
A hyperechoic membrane tethered to the optic disc and extending toward the ora suggests retinal detachment; mobile low-level echoes suggest vitreous hemorrhage.
A focused ocular ultrasound is not a substitute for urgent ophthalmology and stroke-system evaluation.
Interpretation Checklist
Confirm the indication and screen for open-globe risk; do not compress a potentially ruptured globe.
Identify the globe, lens, optic nerve, posterior wall, and vitreous in two planes.
Examine for retinal detachment, vitreous hemorrhage, lens displacement, intraocular foreign body, and gross globe rupture.
If Doppler is available and expertise is adequate, locate the central retinal artery near the optic nerve and compare flow with the opposite eye; interpret absent or reduced flow cautiously.
Correlate with acuity, RAPD, fundus examination, symptom onset, and neurologic findings.
Communicate immediately with ophthalmology and activate the appropriate stroke/vascular pathway when CRAO is suspected, regardless of ultrasound results.
Retrieval Prompt
Does absent central retinal artery flow on ocular Doppler confirm CRAO by itself? → No. It is supportive but technically limited; CRAO remains a clinical emergency requiring specialist and vascular evaluation.
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
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. What’s the diagnosis, and the first move?
Check your answer
Sodium Channel Blocker Toxicity. 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.
From the September 10 edition
Today, three days ago: Lorazepam. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
Seizure/status: 0.1 mg/kg IV, usual max 4 mg per dose, may repeat once. Alcohol withdrawal/agitation: commonly 1–4 mg IV/PO/IM titrated to severity. Severe respiratory depression without airway support, acute narrow-angle glaucoma, hypersensitivity.
From the September 3 edition
A 29-year-old has severe tooth pain but no fever, facial swelling, gingival fluctuance, trismus, or systemic symptoms. Which is the best ED management?
AAmoxicillin-clavulanate for 10 days
BImmediate CT of the neck with contrast
CNSAID plus acetaminophen and urgent dental referral
DIncision and drainage of the painful tooth
Reveal answer
Correct · C
Uncomplicated pulpitis or localized dental pain is treated with analgesia and definitive dental care, not routine antibiotics or imaging. Antibiotics are reserved for spreading infection or systemic involvement.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Prioritize airway, vision, and hemorrhage over CT scans when managing facial trauma in the ED. Master essential bedside exam tactics to protect function. The post Facial Trauma: Approach, Pearls, and Pitfalls appeared first on ACEP Now .
Pros include shorter waits, more time with patients, and reduced burnout. Click through to learn more. The post Concierge Emergency Medicine Offers Multitude of Benefits appeared first on ACEP Now .
Podcast Picks
Two for the shift
Critical Care Perspectives in Emergency Medicine2026-09-01
Brain damage and death from ischemic encephalopathy is common after cardiac arrest. Animal studies and limited observational studies suggest that high oxygen exposure after ROSC may result in neuronal death. As such, it is hypothesized that limiting oxygen exposure (conservative oxygen) many attenuate reperfusion injury and improve outcomes. At present,...
Source
Critical Care Perspectives in Emergency Medicine
Published
2026-09-01
Host
Critical Care Perspectives in Emergency Medicine, Critical Care Perspectives in Emergency Medicine
In this month’s EM Quick Hits Podcast, Amna Karabegovic joins us for an EMC² case of pediatric altered LOA and neurocritical care, Anand Swaminathan simplifies the high-risk management of pulmonary hypertension and...
Annals Journal Watch
From the specialty flagship
One recent paper from Annals of Emergency Medicine worth knowing on shift, chosen for practice impact — independent of today’s topics.
DiBello J, Swaminathan AK, Freeman B · PMID 42476696
A journal club critically appraising thrombolysis for central retinal artery occlusion addresses a time-sensitive but evidence-uncertain ED treatment decision. Residents should understand both the stroke-level urgency of sudden monocular vision loss and the limitations of the data supporting lysis.
Bottom line → Activate your local stroke and ophthalmology pathway immediately for suspected central retinal artery occlusion, but use thrombolysis only through an established protocol and specialist-guided risk-benefit discussion.
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
Pseudofracture mimics can complicate foot and ankle radiographs; recognizing normal lucencies and contour variants helps prevent overcalling metatarsal or talar fractures.
There are multiple reasons why lucent lines may appear in bones, or why bone contours may appear abnormal, mimicking fractures.
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
Metronidazole
Nitroimidazole antimicrobial
Indication
Anaerobic coverage for intra-abdominal, pelvic, dental, and aspiration-related infections; bacterial vaginosis; trichomoniasis; adjunctive therapy in selected C. difficile contexts per local protocols.
What’s your dose? — reveal dosing & cautions
ED Dose
500 mg IV/PO q8–12h for most anaerobic infections. Trichomoniasis: 500 mg PO q12h x 7 days for women or 2 g PO once in selected regimens.
Renal Adjustment
No adjustment for mild-moderate renal impairment; metabolites accumulate in ESRD but single ED doses usually do not require adjustment. Reduce/avoid prolonged dosing in severe hepatic impairment.
Contraindications
Known hypersensitivity; avoid alcohol during therapy and for at least 3 days after due to disulfiram-like reaction risk.
Nausea, metallic taste, neuropathy with prolonged use, hepatic disease, INR when on warfarin.
ED Pearl
Metronidazole is anaerobic coverage, not broad gram-negative coverage — pair it with a gram-negative agent when treating intra-abdominal sepsis unless the companion drug already covers anaerobes.
Sodium channel blocker toxicity with QRS widening, severe hyperkalemia temporization in acidemic patients, selected severe metabolic acidosis, and cardiac arrest special circumstances.
What’s your dose? — reveal dosing & cautions
ED Dose
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.
Renal Adjustment
No simple adjustment; risk of sodium/volume overload is higher in renal failure. Use with close monitoring.
Contraindications
Severe alkalemia, hypocalcemia-related tetany, sodium/volume overload caution.
Interactions
Alkalinization changes distribution/excretion of weak acids/bases; may reduce ionized calcium; incompatible with some IV meds when mixed.
ED Pearl
In TCA toxicity, bicarb is a sodium-channel antidote endpointed to QRS narrowing — do not give one amp and walk away while the QRS stays wide.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Rhythm
Fusion Beats
A single hybrid complex, intermediate between the patient's narrow and wide beats, proves two pacemakers are firing at once — and helps nail a wide tachycardia as VT.
The Tracing
A 66-year-old man is being monitored during a run of regular wide-complex tachycardia. Scanning the strip, most of the beats are broad and uniform, but one complex stands out: it is neither as narrow as his baseline conducted beats nor as wide as the surrounding ectopics, sitting midway in both width and shape. A couple of beats nearby look fully narrow and normally conducted, as if the supraventricular impulse briefly won out. That single in-between complex is the clue — a supraventricular and a ventricular impulse have collided to stamp out one blended morphology on the tracing.
A hybrid QRS of intermediate width and morphology between the supraventricular and the ventricular complexes
Indicates two pacemaker foci firing simultaneously — a supraventricular pacemaker (e.g. sinus node) and a competing ventricular focus
Often seen alongside capture beats (fully conducted narrow beats) in the same strip
Occurs in the setting of ventricular tachycardia and accelerated idioventricular rhythm (AIVR)
Pearls
A fusion beat is physical proof of AV dissociation — a supraventricular and a ventricular impulse depolarized the ventricle together — which is why it helps confirm VT over SVT with aberrancy.
Look for fusion and capture beats together: capture beats are fully conducted narrow complexes, fusion beats are the intermediate blends, and both mark a competing ventricular focus.
Fusion beats aren't inherently dangerous themselves; their value is diagnostic, telling you which rhythm you're actually dealing with. (Dressler first described the beat in 1952.)
Pitfalls
Mistaking a fusion or capture beat for an artifact or an isolated ectopic, and missing the AV-dissociation clue that points to VT.
Assuming a fusion beat always means VT — it also appears in the benign AIVR, so interpret it against rate and clinical context.
Expecting fusion beats to be present in every VT; their absence does not exclude VT, it just removes one confirmatory clue.
At the Bedside
Use a fusion beat as confirmatory evidence when classifying a wide-complex tachycardia: it supports a ventricular origin and pushes you toward treating the rhythm as VT rather than SVT with aberrancy. Weigh it with the rate — the same finding in a slow, well-tolerated rhythm points to AIVR instead.
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 · METATARSAL FRACTURES AND DISLOCATIONS
Self-Examination
Test Your Understanding
A patient has plantar ecchymosis and midfoot pain after axial loading. Non-weight-bearing radiographs are equivocal. What is the best next diagnostic step?
ADischarge with an ankle brace
BCT of the foot
CImmediate MRI of the ankle
DRepeat radiographs in 6 weeks
Reveal answer
Correct answer · B
CT of the foot. CT identifies subtle fractures and tarsometatarsal malalignment when plain films are nondiagnostic. Lisfranc injury should not be dismissed as a sprain based on equivocal non-weight-bearing films.
Study Pace4 topics today; Issue 61 of 94 — Orthopedics / Ophthalmology (Weeks 33 B-35 A)Deadline · June 1, 2026