The Daily Differential — Monday, May 4, 2026

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Myasthenia Gravis

MG can cause rapidly progressive respiratory failure with deceptively normal oxygen saturation until late. ED recognition of myasthenic crisis and avoidance...

At the Bedside

Pathophysiology
Autoimmune antibodies impair postsynaptic acetylcholine receptors or related NMJ proteins.
Weakness worsens with use and improves with rest.
Classic symptoms
Ptosis, diplopia, dysarthria, dysphagia, chewing fatigue, neck flexor weakness, proximal limb weakness.
Sensation and reflexes are usually normal.
Myasthenic crisis
Respiratory failure from diaphragmatic/intercostal/bulbar weakness.
Triggers: infection, surgery, pregnancy/postpartum, medication changes, steroid initiation, heat, stress, antibiotics, magnesium.
ED assessment
ABCs, bedside swallow screen, aspiration risk.
Serial respiratory mechanics:
FVC <15–20 mL/kg, NIF weaker than −20 cm H₂O, inability to count to 20, weak cough, or bulbar symptoms = high risk.
Pulse ox may remain normal until late; do not be reassured by SpO₂ alone.
Labs/imaging to find trigger: CBC, CMP, Mg/phos, UA, CXR, viral testing as indicated, ABG/VBG if ventilatory concern.
Airway
Intubate early for bulbar dysfunction, poor secretion control, hypercapnia, rapidly falling FVC/NIF, or exhaustion.
Avoid prolonged NIV if significant bulbar weakness/aspiration risk.
Neuromuscular blockers:
MG patients are sensitive to nondepolarizing agents; use reduced dosing if needed.
Succinylcholine response is unpredictable and may be prolonged, especially if on pyridostigmine.
Definitive crisis therapy
Neurology/ICU consult.
IVIG or plasma exchange are main therapies for crisis.
Treat infection or trigger.
Steroids may be needed but can transiently worsen weakness; usually coordinate with neurology/ICU.
Cholinergic crisis
Rare; from excess acetylcholinesterase inhibitor.
Findings: weakness plus muscarinic symptoms — salivation, lacrimation, diarrhea, bronchorrhea, bradycardia, miosis.
Management: hold pyridostigmine, supportive care, atropine for severe muscarinic toxicity.

A Classic Presentation

A 34-year-old woman with known MG presents with fever, cough, worsening ptosis, dysphagia, and shortness of breath. She can only count to 8 on one breath, has a weak cough, and her FVC is 12 mL/kg. CXR shows pneumonia. She is intubated early, started on antibiotics, admitted to ICU, and treated with IVIG after neurology consultation.

Study Directive

Memorize ED airway thresholds: FVC <15–20 mL/kg, NIF weaker than −20 cm H₂O, weak cough, bulbar dysfunction.
Make a personal “avoid in MG” medication list and review it before prescribing antibiotics.
Compare myasthenic crisis vs cholinergic crisis from memory, including pupil/secretions/GI findings.
Review one ICU/neurology protocol for IVIG and plasma exchange.

Key Medications

Pyridostigmine: typical chronic adult dose 30–60 mg PO q4–6 hr while awake; dosing individualized. Often held temporarily if intubated due to secretions — coordinate with neurology.
IVIG: 2 g/kg total, commonly 0.4 g/kg/day IV for 5 days or divided over 2–5 days. Check institutional protocol.
Plasma exchange: usually 5 exchanges over 7–14 days; ICU/neurology-directed.
Atropine for severe cholinergic symptoms: 0.5–1 mg IV q3–5 min as needed for bradycardia/bronchorrhea; titrate to drying/HR.
RSI considerations:
- Etomidate: 0.3 mg/kg IV.
- Ketamine: 1–2 mg/kg IV.
- Rocuronium: reduced dose may be considered due to sensitivity; exact dose varies — discuss with pharmacy/anesthesia if time permits.
- Have ventilatory plan and consider sugammadex availability if rocuronium used.

High-Yield Pearls

MG causes fatigable motor weakness with normal sensation and usually normal reflexes.
Respiratory mechanics beat pulse ox for detecting impending crisis.
Avoid MG-worsening drugs: magnesium, aminoglycosides, fluoroquinolones, macrolides, beta blockers, calcium channel blockers, and some antiarrhythmics when possible.

Board Question

A patient with MG presents with worsening weakness and dyspnea. Which finding best indicates need for ICU-level airway concern?

ANormal oxygen saturation
BFVC 12 mL/kg
CPtosis that improves with ice pack
DNormal deep tendon reflexes

Reveal answer

Correct: B

FVC <15–20 mL/kg suggests impending ventilatory failure in MG. Oxygen saturation may remain normal until late because the problem is ventilation and muscle fatigue, not primary oxygenation.

Recent Literature

Review or guideline Ocular myasthenia gravis: a review and practical guide for clinicians
Clin Exp Optom, 2022 · cited 32×
Recent clinical Chimeric Antigen Receptor T-Cells in Myasthenia Gravis: Advances, Safety Challenges, and Future Directions
Muscle Nerve, 2026

Full text · open access

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Peripheral Nerve Disorders

Peripheral nerve complaints are common, but the ED priority is distinguishing benign compressive neuropathies from central lesions, spinal cord/cauda equina...

At the Bedside

Localization first
Central signs: aphasia, neglect, visual field cut, hyperreflexia, spasticity, pronator drift, crossed findings → evaluate for stroke/CNS lesion.
Peripheral nerve: sensory/motor deficit in a nerve distribution, lower motor neuron weakness, decreased reflexes.
Root/radiculopathy: dermatomal pain/sensory loss, myotomal weakness, reflex change, neck/back pain.
Polyneuropathy: symmetric distal sensory loss, burning pain, stocking-glove pattern.
Key ED history
Onset: sudden vs progressive.
Trauma/compression: “Saturday night palsy,” crutch use, prolonged immobilization, laceration.
Pain: radicular, ischemic, compartment syndrome, zoster.
Systemic symptoms: fever, weight loss, cancer, diabetes, renal failure, alcohol use, toxin/medication exposure.
Weakness progression, autonomic symptoms, respiratory symptoms — think GBS.
Focused exam
Motor testing by nerve/root:
Radial nerve: wrist/finger extension.
Median nerve: thumb opposition, thenar strength, first 3.5 digits sensation.
Ulnar nerve: finger abduction/adduction, fifth digit sensation.
Peroneal nerve: dorsiflexion/eversion, dorsal foot sensation.
Tibial nerve: plantarflexion/inversion, sole sensation.
Reflexes: biceps C5/6, brachioradialis C6, triceps C7, patellar L4, Achilles S1.
Vascular exam and compartment assessment when limb symptoms are acute/painful.
Important diagnoses
Bell palsy: unilateral LMN facial weakness including forehead; no other neuro deficits.
Radial neuropathy: wrist drop after compression; splint and outpatient follow-up if no trauma/red flags.
Carpal tunnel: median neuropathy, nocturnal paresthesias, thenar weakness late.
Peroneal neuropathy: foot drop after fibular head compression; check for stroke, L5 radiculopathy, trauma.
Guillain-Barré syndrome: progressive symmetric weakness, paresthesias, areflexia, autonomic instability; may ascend and cause respiratory failure.
Zoster neuropathy: dermatomal pain/rash; motor weakness possible.
Diagnostics
Many isolated compressive neuropathies require no ED imaging if classic and atraumatic.
CT/MRI brain if central signs, acute stroke mimic concern, facial palsy sparing forehead, multiple cranial nerves, or atypical features.
MRI spine for cauda equina, cord compression, epidural abscess/hematoma, severe/progressive radiculopathy with red flags.
Labs for polyneuropathy when indicated: glucose, electrolytes, B12, TSH, renal/liver function, HIV/syphilis depending context.
Suspected GBS: admit; consider FVC/NIF, telemetry, LP/MRI as inpatient/consult-directed.
Management
Remove compression, splint functional position, analgesia, PT/OT referral.
Bell palsy: eye protection plus early steroids; antivirals for severe palsy or possible HSV/VZV.
GBS: ICU/stepdown depending respiratory/autonomic status; IVIG or plasma exchange; avoid steroids as sole therapy.
Urgent specialist involvement for traumatic nerve transection, open injuries, compartment syndrome, rapidly progressive weakness, respiratory compromise, or cauda equina.

A Classic Presentation

A 46-year-old man wakes after sleeping intoxicated over a chair with inability to extend his wrist and numbness over the dorsal first web space. He has intact speech, face, leg strength, and pulses. Exam localizes to radial nerve compression. He receives a wrist extension splint, analgesics, return precautions for progression, and outpatient neurology/hand follow-up.

Study Directive

Draw median, ulnar, radial, peroneal, and tibial nerve motor/sensory territories from memory.
Practice localizing 5 cases: wrist drop, foot drop, facial droop, hand numbness, ascending weakness.
Memorize ED red flags requiring imaging/admission: central signs, bowel/bladder dysfunction, saddle anesthesia, fever/back pain, cancer, progressive bilateral weakness, respiratory symptoms.
Review Bell palsy treatment timing and eye-care instructions.

Key Medications

Bell palsy prednisone: 60–80 mg PO daily for 5–7 days, often followed by short taper; best within 72 hr.
Valacyclovir for Bell palsy adjunct/severe cases: 1 g PO TID x 7 days.
Acyclovir alternative: 400 mg PO five times daily x 7–10 days.
Zoster antiviral: valacyclovir 1 g PO TID x 7 days; adjust for renal function.
Neuropathic pain adjunct: gabapentin often starts 100–300 mg PO TID, titrate; dose-adjust renal function and counsel sedation. Dosing varies widely — check reference.
NSAID example: ibuprofen 400–600 mg PO q6–8 hr PRN; avoid/adjust in renal disease, GI bleed risk, anticoagulation.
GBS IVIG: 0.4 g/kg/day IV x 5 days; inpatient/neurology-directed.

High-Yield Pearls

Forehead sparing suggests a central facial palsy; forehead involvement suggests peripheral CN VII palsy.
Foot drop is not always peroneal neuropathy — consider L5 radiculopathy and stroke if localization is unclear.
GBS is a peripheral nerve disorder that kills through respiratory failure and autonomic instability, not sensory symptoms.

Board Question

A 59-year-old man presents with acute unilateral facial weakness. He cannot wrinkle his forehead, close his eye tightly, or smile on the affected side. No limb weakness, aphasia, or ataxia is present. Best initial treatment?

AAlteplase
BPrednisone and eye protection
CEmergent carotid endarterectomy
DHigh-dose IV methylprednisolone for multiple sclerosis

Reveal answer

Correct: B

Complete unilateral facial weakness including the forehead suggests peripheral CN VII palsy. ED treatment includes eye lubrication/protection and corticosteroids, ideally within 72 hours.

Recent Literature

Review or guideline Autonomic neuropathies
Muscle Nerve, 2021 · cited 57×

Full text · open access
Recent clinical Application and prospects of brain-computer interface technology for motor function reconstruction after brachial plexus injury
Ann Med, 2026

Full text · open access

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Opioid Dependence and Abuse

Opioid use disorder is common and lethal, but ED clinicians can immediately prevent death with naloxone, treat withdrawal, initiate buprenorphine, and...

At the Bedside

Opioid intoxication
Classic triad: CNS depression, respiratory depression, miosis.
Also consider hypoglycemia, head trauma, sedatives, clonidine, organophosphates, carbon monoxide, sepsis.
Prioritize ventilation: airway positioning, BVM, oxygen, capnography.
Naloxone is for reversing respiratory depression, not necessarily fully waking the patient.
Naloxone strategy
Use low titrated doses for opioid-dependent patients if ventilating adequately to avoid severe precipitated withdrawal.
Use larger doses for apnea, severe hypoventilation, or suspected fentanyl/high-potency synthetic exposure.
Observe after reversal; duration depends on opioid involved, naloxone dose, coingestants, recurrent sedation risk, and social safety.
Opioid withdrawal
Symptoms: anxiety, yawning, lacrimation, rhinorrhea, piloerection, myalgias, abdominal cramping, diarrhea, vomiting, tachycardia, hypertension, dilated pupils.
Not usually life-threatening, but very uncomfortable and drives return to use.
Use COWS score to quantify withdrawal.
Buprenorphine initiation
Best when patient has moderate withdrawal, commonly COWS ≥8–12, to reduce risk of precipitated withdrawal.
Especially useful after short-acting opioid use when sufficient time has passed since last use.
For fentanyl exposure, precipitated withdrawal risk is higher; consider longer observation, lower-dose strategies, or local protocol.
OUD care bundle
Offer buprenorphine, naloxone kit/prescription, harm reduction counseling, HIV/HCV testing referral, wound care if injection use, and rapid follow-up.
Screen for pregnancy; pregnancy changes medication planning but OUD treatment remains essential.
Assess suicidality, polysubstance use, housing/safety, and infectious complications.
Disposition
Discharge if stable after observation, normal mental status/ventilation, no dangerous coingestion, and safe plan.
Admit for recurrent respiratory depression, long-acting opioid overdose, methadone toxicity, severe hypoxia/aspiration, pulmonary edema, trauma, infection, or suicidality.

A Classic Presentation

A 27-year-old man is brought in somnolent with RR 6, pinpoint pupils, and SpO₂ 84% after suspected fentanyl use. He is ventilated with BVM and receives naloxone 0.4 mg IV with improved respirations. After observation he develops yawning, myalgias, diarrhea, piloerection, and COWS 14. He is started on buprenorphine/naloxone 8 mg SL, given take-home naloxone, and linked to next-day addiction follow-up.

Study Directive

Practice a naloxone escalation algorithm for two scenarios: apneic patient vs opioid-dependent but breathing patient.
Memorize COWS components and your threshold for buprenorphine initiation.
Review your state/institution rules for ED buprenorphine prescribing and bridge prescriptions.
Build a discharge script: naloxone use, not using alone, fentanyl test strips if available, syringe services, and follow-up appointment.

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Mechanism Pearl of the Day: Today’s topics all hinge on localizing failure in the neuro-respiratory axis: ICH disrupts central control and consciousness, MG blocks neuromuscular transmission, peripheral nerve disorders impair signal conduction, and opioids suppress brainstem respiratory drive. The ED question is always: “Where is the lesion, and is ventilation threatened?”

Key Medications

Naloxone IV titration: 0.04 mg IV initially if opioid-dependent and breathing; repeat/escalate every 2–3 min: 0.04 → 0.1 → 0.2 → 0.4 → 2 mg as needed.
Naloxone for apnea/severe respiratory depression: 0.4–2 mg IV/IM/IN; repeat q2–3 min. Higher cumulative doses may be needed for fentanyl analogs.
Naloxone infusion: use for recurrent respiratory depression; common starting rate is two-thirds of the effective wake-up dose per hour. Titrate to ventilation.
Buprenorphine/naloxone ED induction:
- Initial 4–8 mg SL when moderate withdrawal present.
- Reassess in 30–60 min; repeat 4–8 mg.
- Common ED day-1 total 8–16 mg; some protocols allow up to 24–32 mg, especially fentanyl-era practice — follow local protocol.
Clonidine for withdrawal symptoms: 0.1 mg PO q6–8 hr PRN; monitor BP, hold for hypotension/bradycardia.
Ondansetron: 4 mg PO/IV q6–8 hr PRN nausea.
Loperamide: 4 mg PO once, then 2 mg after loose stools; max 8 mg/day OTC or 16 mg/day Rx.
Ibuprofen: 400–600 mg PO q6–8 hr PRN myalgias if no contraindications.
Acetaminophen: 650–1,000 mg PO q6–8 hr PRN; max generally 3,000–4,000 mg/day depending risk factors.

High-Yield Pearls

Naloxone’s goal is adequate ventilation, not a fully awake and angry patient.
Buprenorphine can precipitate withdrawal if given before sufficient spontaneous withdrawal has developed.
ED-initiated buprenorphine improves treatment engagement and reduces illicit opioid use compared with referral alone.

Board Question

A heroin-dependent patient with opioid overdose is breathing 6/min but has a pulse. What is the best immediate ED action?

AWait for toxicology results
BProvide ventilatory support and titrated naloxone
CGive flumazenil
DGive buprenorphine immediately while unconscious

Reveal answer

Correct: B

Opioid overdose kills by respiratory depression, so ventilation comes first, followed by naloxone titrated to adequate respirations. Buprenorphine is for awake patients in withdrawal, not initial reversal of coma/apnea.

Recent Literature

Review or guideline Historical Review: Opiate Addiction and Opioid Receptors
Cell Transplant, 2019 · cited 168×

Full text · open access
Recent clinical Substance use among incarcerated male population in Freetown, Sierra Leone: Prevalence, predictors, and risk profiles using the WHO ASSIST
Glob Public Health, 2026

Full text · open access

TheDaily Differential

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At the Bedside

Study Directive

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Peripheral Nerve Disorders

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