When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EMERGENTNeurology

Myasthenic Crisis

Myasthenia gravis exacerbation with respiratory failure requiring intubation. Triggered by infection, surgery, medication changes, or drug interactions. Same respiratory monitoring as GBS -FVC < 20 → intubate. Know the drugs that worsen MG.

🔍 Overview

Myasthenia Gravis -Key Concepts

Autoantibodies against AChR (acetylcholine receptor) at the neuromuscular junction → fatigable weakness
Fatigable: weakness worsens with repeated use and improves with rest. Worse at end of day.
Ocular symptoms (#1 presenting symptom): ptosis, diplopia -often asymmetric
Generalized MG: proximal limb weakness, bulbar symptoms (dysphagia, dysarthria, nasal voice), respiratory failure
Anti-AChR antibodies positive in ~85% of generalized MG. Anti-MuSK antibodies in ~5–8% (more bulbar involvement, worse prognosis).
CT chest for thymoma -present in ~15% of MG patients. Thymectomy recommended for thymoma and for non-thymomatous generalized AChR+ MG age 18–65.

Drugs That Worsen MG -MUST KNOW

These drugs can precipitate myasthenic crisis. Avoid in all MG patients:

Drug Class	Specific Agents
Antibiotics	Aminoglycosides (gentamicin, tobramycin), fluoroquinolones, macrolides (azithromycin -controversial), tetracyclines
Cardiac	Beta-blockers, calcium channel blockers, procainamide, quinidine
Neuromuscular blockers	Avoid succinylcholine (unpredictable response). Use non-depolarizing agents with caution (increased sensitivity → prolonged paralysis).
Other	Magnesium (blocks NMJ -avoid IV Mg unless life-threatening indication), D-penicillamine, checkpoint inhibitors, botulinum toxin, lithium

Myasthenic Crisis vs Cholinergic Crisis

Feature	Myasthenic Crisis	Cholinergic Crisis
Cause	Disease exacerbation (undertreated)	Pyridostigmine overdose
Pupils	Normal or dilated	Miosis (constricted)
Secretions	Normal	Excessive (SLUDGE: salivation, lacrimation, urination, diarrhea, GI cramping, emesis)
Fasciculations	Absent	Present
Response to edrophonium	Improves	Worsens
Treatment	IVIG or PLEX + immunosuppression	Hold pyridostigmine, atropine for secretions

🚨 Management

Myasthenic Crisis Treatment

Respiratory

FVC + NIF q4–6h. Same 20/30/40 rule as GBS. Intubate if FVC < 20 mL/kg or NIF < −30. Avoid succinylcholine and minimize non-depolarizing agents. BiPAP can bridge but do NOT delay intubation if deteriorating.

Rapid immunotherapy

IVIG 0.4 g/kg/day × 5 days OR plasmapheresis × 5 exchanges. Both equally effective. PLEX onset is faster (~24–48h) vs IVIG (3–5 days). Choose based on availability and access.

Steroids

Start high-dose steroids (prednisone 1 mg/kg/day or methylprednisolone 1g IV × 3–5 days). Warning: steroids can cause transient worsening in the first 1–2 weeks → always start WITH IVIG/PLEX, not alone in crisis.

Cholinesterase inhibitor

Hold pyridostigmine during crisis (increased secretions worsen respiratory status, and it may contribute to cholinergic crisis). Resume when improving and extubated.

Trigger

Identify and treat the trigger: infection (#1 -pneumonia, UTI), medication change, surgery, emotional stress. Review medication list for MG-exacerbating drugs.

Chronic MG Management

Drug	Role	Notes
Pyridostigmine (Mestinon) SYMPTOMATIC	AChE inhibitor -increases ACh at NMJ	First-line symptomatic treatment. 60 mg PO TID, titrate. Does NOT alter disease course -only improves symptoms.
Prednisone (Deltasone)	Immunosuppression	Most patients need immunosuppression beyond pyridostigmine. Start low, escalate slowly (risk of initial worsening).
Azathioprine (Imuran)	Steroid-sparing agent	Takes 6–12 months to work. Check TPMT before starting (deficiency → myelosuppression).
Mycophenolate (CellCept)	Steroid-sparing agent	Alternative to azathioprine. Common choice. Teratogenic.
Rituximab (Rituxan)	Anti-CD20 -refractory MG	Especially effective in anti-MuSK MG. Growing evidence for AChR+ refractory disease.
Efgartigimod (Vyvgart)	FcRn inhibitor -reduces pathogenic IgG	ADAPT, 2021: improved MG-ADL by ≥ 2 points in 67.7% vs 29.7% placebo. IV infusion cycles.
Thymectomy	Surgical -removes pathogenic antigen source	Indicated if thymoma. Also beneficial in AChR+ non-thymomatous MG < 65 yrs (MGTX, 2016). Response takes months.

🧪 Workup

Workup

AChR Ab (~85%)
MuSK Ab if AChR neg
CT chest -thymoma
PFTs (FVC, NIF)
Ice pack test -ptosis improvement

💊 Medications

Medications

Drug	Dose	Route	Notes
Pyridostigmine	60mg q4-6h	PO	AChE inhibitor
Prednisone	Start low, titrate	PO	Can worsen MG initially
Azathioprine	2-3mg/kg/day	PO	Steroid-sparing
IVIG	0.4g/kg×5d	IV	Crisis
Rituximab	375mg/m²	IV	Refractory

📋 On Rounds

Why should you avoid IV magnesium in myasthenia gravis?

Magnesium acts as a calcium channel blocker at the neuromuscular junction -it inhibits presynaptic calcium-dependent acetylcholine release and reduces postsynaptic sensitivity to ACh. In a patient with MG (where ACh receptor density is already reduced by autoantibodies), adding magnesium further impairs neuromuscular transmission → can precipitate myasthenic crisis and respiratory failure.

What medications are contraindicated in myasthenia gravis and why?

Several common medications can precipitate or worsen myasthenic crisis by impairing neuromuscular transmission: (1) Aminoglycosides (gentamicin, tobramycin) -block presynaptic Ca²⁺ channels → reduced ACh release. (2) Fluoroquinolones -same mechanism, plus direct NMJ blockade. (3) Beta-blockers -impair NMJ safety factor. (4) Magnesium -blocks presynaptic Ca²⁺ channels (don't aggressively replete Mg in MG patients).

What is cholinergic crisis and how do you differentiate it from myasthenic crisis?

Both present with weakness and respiratory failure, but the mechanism is opposite. Myasthenic crisis: under-treated MG → insufficient ACh at NMJ → weakness. Pupils: normal or dilated. Secretions: dry. Responds to: edrophonium/neostigmine (improves). Cholinergic crisis: over-treated with pyridostigmine → excess ACh → depolarization block + muscarinic effects. Pupils: miotic (small).

How do you differentiate MG from Lambert-Eaton syndrome?

MG: autoantibodies against post-synaptic AChR → fatigable weakness that WORSENS with repetitive use, proximal > distal, bulbar symptoms (ptosis, diplopia, dysphagia) prominent, reflexes normal. EMG: decremental response on repetitive nerve stimulation. Lambert-Eaton (LEMS): autoantibodies against pre-synaptic voltage-gated calcium channels (P/Q type)

Clinical Examples

📋 Case 1, Myasthenic Crisis

Patient: 58F with known AChR Ab+ MG on pyridostigmine 60 mg QID. Admitted with worsening dyspnea and dysphagia after UTI (treated with ciprofloxacin). FVC 14 mL/kg (declining). Bilateral ptosis, weak neck flexion, nasal speech.

Key findings: Myasthenic crisis: respiratory failure from MG exacerbation. Triggered by UTI (infection is #1 precipitant) + ciprofloxacin (fluoroquinolones worsen NMJ transmission). FVC < 20 = intubation threshold.

Management:

ICU admission, check FVC q4h (same monitoring protocol as GBS)
IVIG 0.4 g/kg/day × 5 days OR PLEX q other day × 5 sessions (both equally effective)
STOP ciprofloxacin, switch to a non-NMJ-affecting antibiotic (ceftriaxone, TMP-SMX)
HOLD pyridostigmine during crisis (excess secretions complicate airway management)
Intubate if FVC < 15 mL/kg, declining rapidly, or unable to handle secretions, use non-depolarizing NMB (avoid succinylcholine, MG patients are resistant)

Teaching point: The most common trigger for myasthenic crisis is infection, not medication non-compliance. Always review the med list, fluoroquinolones, aminoglycosides, beta-blockers, and magnesium can precipitate crisis. The MG medication "hit list" should be at every bedside.

📋 Case 2, New Diagnosis of MG with Thymoma

Patient: 45M with 3 months of fluctuating diplopia, ptosis (worse in evening), difficulty chewing steak. Ice pack test: ptosis improves bilaterally. AChR antibodies positive. CT chest: anterior mediastinal mass 4 cm.

Key findings: New MG with thymoma, ~15% of MG patients have thymoma, and ~30% of thymoma patients develop MG. Thymectomy is indicated for ALL thymomas regardless of MG severity, plus for non-thymomatous MG per MGTX trial.

Management:

Start pyridostigmine 60 mg PO TID (symptomatic relief, first-line)
CT-guided biopsy of mediastinal mass → staging
Thymectomy: robotic or open, both curative for thymoma + improves MG outcomes MGTX, 2016
Pre-op optimization: may need IVIG or PLEX before surgery (reduce perioperative myasthenic crisis risk)
Start prednisone LOW (10 mg, titrate up slowly), high-dose steroids can transiently worsen MG in first 2 weeks

Teaching point: Always get CT chest in new MG, thymoma is present in 15%. The MGTX trial showed thymectomy improves outcomes even in NON-thymomatous MG (AChR Ab+, age 18-65). Prednisone must be started low and titrated slowly to avoid initial worsening.

📋 Case 3, MuSK-Positive MG

Patient: 32F with prominent bulbar symptoms: severe dysphagia, dysarthria, facial weakness, tongue atrophy. Minimal limb involvement. AChR antibodies NEGATIVE. MuSK antibodies POSITIVE. Failed pyridostigmine (made worse).

Key findings: MuSK-positive MG, distinct phenotype: bulbar and facial predominance, tongue/facial atrophy, poor response to pyridostigmine (often makes symptoms worse), and no benefit from thymectomy.

Management:

Stop pyridostigmine (MuSK-MG often worsens with AChE inhibitors)
Rituximab is emerging as first-line for MuSK-MG (excellent response rate ~70-80%)
PLEX preferred over IVIG for acute exacerbations (MuSK antibodies are IgG4, not efficiently removed by IVIG)
Prednisone + mycophenolate as standard immunosuppression
No thymectomy (thymoma is extremely rare in MuSK-MG, and thymectomy does not improve outcomes)

Teaching point: MuSK-MG breaks all the rules of AChR-MG: pyridostigmine worsens it, thymectomy doesn't help, IVIG is less effective than PLEX, and rituximab works better than traditional immunosuppressants. Always check MuSK antibodies if AChR is negative.

📣 Sample Presentation

One-Liner

"Mrs. Park is a 60-year-old with AChR Ab+ myasthenia gravis on pyridostigmine who presents with worsening dyspnea and dysphagia after a UTI. FVC 16 mL/kg. Diagnosed with myasthenic crisis."

Key Points to Cover on Rounds

Myasthenic crisis triggered by UTI. FVC 16 mL/kg (<20 → intubated for airway protection). NIF −18 cmH₂O. Treatment: IVIG 0.4 g/kg/day × 5 days. Pyridostigmine HELD during crisis (excess secretions worsen airway). Antibiotics for UTI: switched from ciprofloxacin → ceftriaxone (fluoroquinolones contraindicated in MG). Offending meds reviewed -no aminoglycosides, no BB, no Mg supplementation. Methylprednisolone 1g IV × 3 days (cautious -steroids can transiently worsen MG in first 7-10 days). Plan: daily FVC/NIF, restart pyridostigmine when improving and extubated.

Monitoring

FVC every visit
Med review -avoid aminoglycosides, FQs, BB, Mg
Thymoma surveillance
Infection screening on immunosuppression

⚡ Summary

Summary

Diagnosis

Fatigable weakness (worse with use, better with rest). Ptosis, diplopia, bulbar symptoms. AChR Ab positive (~85%), MuSK Ab in some.

Treatment

Pyridostigmine (symptomatic). Immunosuppression: prednisone → steroid-sparing (azathioprine, mycophenolate, rituximab).

Crisis

FVC < 20 mL/kg → intubate. Hold pyridostigmine. IVIG or PLEX. ICU admission.

Avoid These Meds

Aminoglycosides, fluoroquinolones, beta-blockers, magnesium, telithromycin, D-penicillamine, botulinum toxin. Worsen NMJ transmission.

Thymectomy

Indicated if thymoma (CT chest mandatory). Also improves outcomes in AChR Ab+ MG without thymoma MGTX, 2016.

Cholinergic Crisis

Excess pyridostigmine → SLUDGE symptoms, weakness, miosis. Antidote: atropine. Hold anticholinesterase. Differentiate from myasthenic crisis.

📄 One Pager

Neurology · One Pager

Myasthenia Gravis

Fatigable weakness (worse with use). AChR antibodies. Pyridostigmine for symptoms. IVIG/PLEX for crisis. Avoid aminoglycosides, FQs, BB, Mg. Thymectomy if thymoma.

🧪 Diagnosis

Fluctuating weakness: ptosis, diplopia, bulbar symptoms (dysphagia, dysarthria), proximal limb weakness. AChR Ab positive ~85%. MuSK Ab in some seronegatives. CT chest (thymoma).

🚨 Myasthenic Crisis

FVC < 20 mL/kg → intubate. Hold pyridostigmine (excess secretions). IVIG 0.4 g/kg/day × 5d or PLEX. Identify trigger: infection, surgery, medication change.

⚠️ Dangerous Medications

Aminoglycosides, fluoroquinolones, macrolides, beta-blockers, magnesium IV, D-penicillamine, telithromycin, botulinum toxin. All worsen NMJ transmission.

💊 Key Drugs

Pyridostigmine60 mg q4-6h

PrednisoneStart low, titrate up (can transiently worsen)

Azathioprine2-3 mg/kg/day (steroid-sparing)

IVIG0.4 g/kg × 5d (crisis)

⚠️ Pitfalls

Aminoglycosides or FQs in MG patient → crisis
Not checking FVC (crisis can develop rapidly)
Missing thymoma (CT chest in all new MG)
Cholinergic crisis from pyridostigmine excess (SLUDGE symptoms)