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

Guillain-Barré Syndrome

Acute inflammatory demyelinating polyneuropathy -ascending weakness 1–4 weeks after infection. 30% need intubation. The key danger: respiratory failure from diaphragm weakness. Monitor NIF and FVC serially. Do NOT wait for ABG to deteriorate -intubate early.

🔍 Overview

Clinical Features

Ascending symmetric weakness -starts in legs, progresses to arms, trunk, respiratory muscles, cranial nerves
Areflexia or hyporeflexia -characteristic finding
Preceded by infection 1–4 weeks prior in ~70%: Campylobacter jejuni (#1), CMV, EBV, HIV, Mycoplasma, Zika
Autonomic dysfunction (~70%): labile BP, tachycardia, bradycardia, arrhythmias, urinary retention, ileus
Neuropathic pain (~60%) -may be the presenting symptom before weakness
Facial weakness bilateral (facial diplegia) in ~50%. Bulbar weakness → dysphagia, aspiration risk.

Diagnosis

Test	Findings
CSF (LP)	Albuminocytologic dissociation: elevated protein (> 45 mg/dL) with normal WBC (< 10). May be normal in first week. If WBC > 50 → think HIV, Lyme, sarcoidosis, or lymphomatous meningitis.
Nerve conduction studies / EMG	Demyelination pattern: prolonged distal latencies, conduction block, slowed conduction velocity, absent F waves. May be normal first few days. Repeat at 2 weeks if initially normal.
Anti-ganglioside antibodies	Anti-GM1 (AMAN variant), anti-GQ1b (Miller Fisher -ophthalmoplegia + ataxia + areflexia). Not required for diagnosis.

Respiratory Monitoring -The 20/30/40 Rule

Intubate if ANY of: FVC < 20 mL/kg, NIF < −30 cmH₂O, or FVC decline > 30% from baseline. Do NOT wait for hypercapnia or hypoxia on ABG -by then it's too late. Check FVC and NIF q4–6h in all GBS patients.

The Erasmus GBS Respiratory Insufficiency Score (EGRIS) predicts need for ventilation: rapid progression, high disability score at admission, and facial/bulbar weakness are the strongest predictors.

🚨 Management

Immunotherapy

Treatment	Dose	Notes
IVIG 1ST LINE	0.4 g/kg/day IV × 5 days	Equivalent efficacy to plasmapheresis. Easier to administer. Side effects: headache, renal failure (check IgA first -IgA-deficient patients get anaphylaxis), aseptic meningitis, thromboembolic events. GBS IVIG Trial, 1992
Plasmapheresis (PLEX) EQUIVALENT	5 exchanges over 2 weeks	Equivalent to IVIG. Preferred if IVIG contraindicated. Requires large-bore central access. More hemodynamic effects. Guillain-Barré Syndrome Study Group, 1985

Do NOT give both IVIG and PLEX -PLEX removes the IVIG you just gave. Pick one. Do NOT give corticosteroids -no benefit in GBS (unlike in CIDP or myasthenia).

Supportive Care

ICU admission for all moderate-severe GBS (rapid progression, bulbar involvement, autonomic dysfunction)
FVC + NIF q4–6h -trend is more important than single values
DVT prophylaxis -immobile patient, high VTE risk. Enoxaparin + SCDs.
Pain management -gabapentin or pregabalin for neuropathic pain. Opioids if severe. Pain is often undertreated.
Autonomic monitoring -telemetry (bradycardia, heart block possible). Gentle fluid management (labile BP). Avoid β-blockers (can worsen bradycardia episodes).

📋 On Rounds

Why do you check FVC and not just ABG for respiratory monitoring in GBS?

The ABG is a lagging indicator of respiratory failure in neuromuscular disease. Patients with progressive diaphragm weakness compensate by increasing respiratory rate → they maintain normal PaO₂ and PaCO₂ until they're nearly exhausted. When the CO₂ finally rises on ABG, they're about to arrest. FVC (forced vital capacity) is a leading indicator -it declines progressively as respiratory muscles weaken, well before gas exchange deteriorates.

What is the 20/30/40 rule in GBS and why is FVC more important than SpO₂?

The 20/30/40 rule predicts the need for intubation: FVC < 20 mL/kg, NIF < −30 cmH₂O, or FVC decline > 30% from baseline. Additionally, bulbar dysfunction (inability to swallow, weak cough) independently warrants intubation. SpO₂ is a late and unreliable sign -a patient with GBS can have normal SpO₂ until minutes before respiratory arrest because their lungs are normal; the problem is the respiratory muscles.

What are the differences between IVIG and plasmapheresis (PLEX) for GBS?

Both are equally effective -Hughes, 2014 Cochrane showed no significant difference in outcomes. IVIG: 0.4 g/kg/day × 5 days. Advantages: easier to administer, no special equipment, can do on general floor. Disadvantages: headache, aseptic meningitis, renal failure (sucrose-containing formulations), thrombotic events. PLEX: 5 exchanges over 1-2 weeks. Advantages: faster onset of improvement in some studies.

Can you use steroids in GBS?

No -steroids do NOT help GBS and may be harmful. This is a common mistake because GBS is autoimmune and steroids work in many autoimmune conditions. However, multiple RCTs and Cochrane reviews have shown corticosteroids do not improve outcomes and may delay recovery. The reason is unclear -GBS inflammation involves different immune pathways (complement-mediated, macrophage-mediated demyelination) than conditions responsive to steroids.

Clinical Examples

📋 Case 1, Classic AIDP with Respiratory Compromise

Patient: 42M with ascending bilateral leg weakness × 4 days, now unable to walk. Had Campylobacter gastroenteritis 2 weeks ago. Areflexic throughout. Bilateral facial weakness. FVC 22 mL/kg (declining from 30 mL/kg 12h ago).

Key findings: Classic GBS (AIDP): ascending weakness + areflexia + preceding infection. FVC < 20 mL/kg = intubation threshold ("20-30-40 rule": FVC < 20, MIP < -30, MEP < 40). FVC trending down = impending respiratory failure.

Management:

ICU admission, check FVC q4-6h (the single most important monitoring parameter)
IVIG 0.4 g/kg/day × 5 days (first-line, equal efficacy to PLEX, easier to administer)
Intubate when FVC < 20 mL/kg or declining rapidly, do NOT wait for hypoxia or hypercapnia
DVT prophylaxis (immobilized), pain management (neuropathic pain is severe, gabapentin), autonomic monitoring (dysautonomia: HR/BP lability)
NO steroids (do not help GBS, may worsen outcome)

Teaching point: Serial FVC is the most critical measurement in GBS, not SpO₂. By the time SpO₂ drops, the patient is in extremis. The "20-30-40 rule" provides objective intubation thresholds. ~30% of GBS patients require mechanical ventilation.

📋 Case 2, Miller Fisher Syndrome

Patient: 55F with 3 days of double vision, unsteady gait, and bilateral ptosis. Areflexia. No limb weakness. Recent URI 2 weeks ago. MRI brain normal.

Key findings: Miller Fisher syndrome triad: ophthalmoplegia + ataxia + areflexia. A GBS variant. Anti-GQ1b antibodies positive in > 90%. Does NOT typically cause limb weakness or respiratory failure (unlike classic GBS).

Management:

IVIG 0.4 g/kg/day × 5 days (standard treatment, though most cases self-resolve)
Check anti-GQ1b antibodies (confirmatory, highly specific for Miller Fisher)
Monitor FVC despite no limb weakness (overlap with GBS can develop, 5-10% progress to AIDP)
LP: albuminocytologic dissociation (elevated protein, normal WBC), same as classic GBS
Prognosis excellent: most recover fully within 2-3 months without residual deficits

Teaching point: Miller Fisher is the most common GBS variant. The triad of ophthalmoplegia + ataxia + areflexia after a viral infection should trigger immediate GQ1b testing and admission for FVC monitoring, even though prognosis is better than classic AIDP.

📋 Case 3, GBS vs CIDP Diagnostic Dilemma

Patient: 60M with progressive proximal and distal weakness over 3 months. Initially diagnosed as GBS 10 weeks ago and treated with IVIG, improved briefly then relapsed. Now wheelchair-bound. Areflexic. No preceding infection.

Key findings: Progression > 8 weeks = by definition NOT GBS (GBS peaks by 4 weeks). This is CIDP (chronic inflammatory demyelinating polyneuropathy). The relapse after IVIG and chronic course are diagnostic clues. CIDP responds to steroids (unlike GBS).

Management:

NCS/EMG: demyelinating pattern (prolonged distal latencies, temporal dispersion, conduction block)
Prednisone 1 mg/kg daily × 4-8 weeks → slow taper (first-line for CIDP, unlike GBS, steroids work)
IVIG 2 g/kg over 2-5 days (alternative first-line, some patients prefer to avoid steroids)
If steroid/IVIG-refractory: PLEX, rituximab, or other immunosuppressants
Long-term maintenance therapy often required (CIDP is chronic, relapsing)

Teaching point: The critical distinction: GBS = monophasic, peaks ≤ 4 weeks, steroids DON'T work. CIDP = chronic/relapsing, progresses > 8 weeks, steroids DO work. Any "GBS" that relapses or progresses beyond 8 weeks should be reclassified as CIDP.

📣 Sample Presentation

One-Liner

"Mr. Fernandez is a 45-year-old presenting with 5 days of ascending bilateral leg weakness and paresthesias following a diarrheal illness 3 weeks ago. Areflexic on exam. FVC 28 mL/kg."

Key Points to Cover on Rounds

GBS -ascending, symmetric, areflexic weakness. Preceding GI illness (likely Campylobacter). FVC 28 mL/kg (concerning -approaching 20/30/40 rule). NIF −35 cmH₂O. LP: protein 120, WBC 3 (albuminocytologic dissociation). NCS/EMG: demyelinating pattern (AIDP). Treatment: IVIG 0.4 g/kg/day × 5 days started today. FVC trending q6h: 28→26 (declining). ICU admission. Plan: if FVC <20 or declining rapidly → intubate. DVT prophylaxis (heparin SQ). PT/OT. Monitor autonomic dysfunction (HR/BP lability).

Monitoring -Guillain-Barre Syndrome

Parameter	Frequency	Target / Action
FVC (forced vital capacity)	q4–6h (the #1 priority)	Intubate if FVC < 20 mL/kg or declining > 30% from baseline. FVC is the vital sign in GBS -do NOT rely on SpO2 or ABG (lagging indicators).
NIF (negative inspiratory force)	q4–6h (with FVC)	Intubate if weaker than -20 to -30 cmH2O. Declining NIF indicates diaphragmatic weakness.
HR / BP (autonomic dysfunction)	Continuous telemetry	Labile BP, tachycardia/bradycardia, arrhythmias in ~70% of GBS. Avoid beta-blockers (can worsen bradycardia episodes). Gentle fluid management for BP lability. Note: this is autonomic dysfunction, not autonomic dysreflexia (which is a spinal cord injury phenomenon).
I&Os (neurogenic bladder)	Strict	Urinary retention is common from autonomic dysfunction. Monitor for distension. May need intermittent catheterization or Foley.
Daily neuro exam	Daily (at minimum)	Track progression: proximal vs distal strength (MRC scale), cranial nerve function, bulbar weakness (swallowing, cough). Nadir typically at 2–4 weeks.
Pain assessment	Each shift	Neuropathic pain in ~60% -often undertreated. Use gabapentin or pregabalin. Opioids if severe.

The 20/30/40 rule: Intubate if FVC < 20 mL/kg, NIF < -30 cmH2O, or FVC decline > 30%. By the time ABG shows respiratory acidosis, you are too late for a controlled intubation.

🧪 Workup

Workup

LP -high protein, normal WBC
NCS/EMG -demyelinating vs axonal
FVC q4-6h -intubate <20mL/kg
NIF -intubate <−30
Anti-ganglioside Ab
MRI spine -rule out cord compression

💊 Medications

Medications -Guillain-Barre Syndrome

Drug	Dose	Route	Notes
IMMUNOTHERAPY (choose ONE)
IVIG PREFERRED	0.4 g/kg/day x 5 days	IV	Preferred due to easier administration. Check IgA level first (IgA-deficient → anaphylaxis risk). Side effects: headache, renal failure, aseptic meningitis, thrombotic events.
Plasma exchange (PLEX)	5 sessions over 2 weeks	IV (large-bore access)	Equivalent efficacy to IVIG. Use if IVIG contraindicated. Requires central access. More hemodynamic effects.
Do NOT combine IVIG + PLEX (PLEX removes IVIG). Steroids are NOT effective in GBS.
SUPPORTIVE CARE
Gabapentin (Neurontin)	100–900 mg TID, titrate up	PO	Neuropathic pain -first-line. Pain is present in ~60% and often undertreated.
Pregabalin (Lyrica)	75–150 mg BID	PO	Alternative to gabapentin for neuropathic pain.
Enoxaparin (Lovenox) MANDATORY	40 mg SQ daily	SQ	DVT prophylaxis is mandatory. Immobile patients at very high VTE risk. Add SCDs. Continue until ambulatory.