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Neuromuscular Emergencies

What Do You Need to Know?

GBS: ascending paralysis + areflexia + albuminocytologic dissociation; IVIg or PLEX (NOT both, NOT steroids); monitor FVC every 4–6 hrs — intubate using the GBS 20/30/40 rule: FVC <20 mL/kg, NIF less negative than −30 cmH₂O, or MEP <40 cmH₂O (distinct from the MG 20/20/20 rule)
Myasthenic crisis: 20/20/20 rule (FVC <20 mL/kg, NIF <−20 cmH₂O, PaCO₂ >50) → intubate; IVIg or PLEX equally effective; know the medication avoidance list
Rhabdomyolysis: CK >5× ULN; aggressive IV NS (target UO >200–300 mL/hr); complications = AKI, hyperkalemia, DIC, compartment syndrome
Critical illness neuromyopathy: failure to wean + flaccid quadriparesis; CIM (normal SNAPs, better prognosis) vs CIP (reduced SNAPs, worse prognosis); prevention > treatment
Acute flaccid paralysis DDx: GBS vs botulism vs tick paralysis vs MG crisis vs CINM vs periodic paralysis vs transverse myelitis vs AFM — reflexes, pupils, sensory exam, and NCS pattern differentiate
NM respiratory failure: FVC is the best single bedside test, but clinical trajectory (rate of decline, work of breathing, bulbar dysfunction, secretion management) and ability to protect the airway matter more than any single FVC value. A patient with a "normal" FVC who is fatiguing, swallowing poorly, or trending down rapidly should be intubated. Conversely, a stable patient just below threshold may not need immediate intubation. Do not rely on SpO₂ alone (late finding); diaphragm weakness → orthopnea, paradoxical breathing.
Toxin-related emergencies: botulism = descending + dilated pupils; organophosphates = SLUDGE + nicotinic (atropine + 2-PAM); black widow = excessive ACh release; tetrodotoxin = Na⁺ channel block

🚩 Don’t Miss — Test-Day Priorities

GBS 20/30/40 rule: FVC <20 mL/kg, MIP less negative than −30 cmH₂O, or MEP <40 cmH₂O → intubate. MG crisis uses the 20/20/20 rule (FVC <20, NIF <−20, PaCO₂ >50).
GBS & MG crisis treatment: IVIG or PLEX (equally effective, NOT both). AVOID steroids in GBS (no benefit, may delay recovery). Steroids are standard in MG.
MG crisis drug triggers: aminoglycosides, fluoroquinolones, β-blockers, IV magnesium, telithromycin, procainamide, neuromuscular blockers — always reviewed on test day.
Botulism: descending paralysis + bulbar onset + dilated/fixed pupils + dry mouth + autonomic dysfunction → equine antitoxin (adults), BabyBIG (IV human botulism Ig) for infant botulism (constipation, poor feeding, descending hypotonia).
NMS vs serotonin syndrome: NMS = neuroleptic + lead-pipe rigidity + hyperthermia + autonomic + CK markedly elevated → stop neuroleptic, dantrolene + bromocriptine. Serotonin syndrome = serotonergic drug + clonus (esp lower extremity) + hyperreflexia + tremor → stop drug, cyproheptadine + benzo.
Malignant hyperthermia: volatile anesthetic or succinylcholine in RYR1 / CACNA1S patient → masseter spasm + rigidity + hyperthermia + hyperkalemia + rhabdo → DANTROLENE + active cooling.
Organophosphate poisoning: SLUDGE-M + miosis + fasciculations + bradycardia + respiratory failure → ATROPINE + PRALIDOXIME (2-PAM). Watch for intermediate syndrome at 24–96 hr (neck flexor, proximal, respiratory weakness) and OPIDN delayed neuropathy 1–3 wk later.
Rhabdomyolysis labs: CK >5× ULN + myoglobinuria; expect HYPERKALEMIA, hyperphosphatemia, HYPOCALCEMIA, elevated uric acid; aggressive IVF; urinary alkalinization controversial; watch for compartment syndrome.
Periodic paralysis attack: hypokalemic → cautious oral/IV KCl + glucose-free fluids; hyperkalemic → oral glucose / IV insulin-dextrose; monitor airway and telemetry.
Tick paralysis: ascending flaccid paralysis mimicking GBS but with normal CSF + reduced CMAP amplitudes — find and remove the tick → rapid resolution. Anti-MDA5 amyopathic DM with rapidly progressive ILD → early aggressive triple immunosuppression.

🔍 Buzzwords & Pathognomonic FindingsClinical · Labs / monitoring · Treatment pearls

Clinical phenotype

Ascending paralysis + areflexia + recent GI/URI infection → GBS (AIDP)
Descending paralysis + dilated pupils + dry mouth + bulbar onset → Botulism
Constipation + poor feeding + floppy infant + descending weakness → Infant botulism
Neuroleptic + lead-pipe rigidity + hyperthermia + autonomic instability → NMS
Serotonergic drug + lower-extremity clonus + hyperreflexia + diaphoresis → Serotonin syndrome
Masseter spasm during induction with volatile anesthetic / succinylcholine → Malignant hyperthermia (RYR1)
SLUDGE-M + miosis + fasciculations + garlic odor in a farmer → Organophosphate poisoning
Ascending flaccid paralysis in a child after a hike, normal CSF → Tick paralysis
Amyopathic DM rash + rapidly progressive hypoxemic ILD → Anti-MDA5 RP-ILD

Labs / monitoring / studies

FVC <20 mL/kg, MIP >−30, MEP <40 cmH₂O → GBS intubation threshold (20/30/40 rule)
FVC <20 mL/kg, NIF <−20, PaCO₂ >50 → Myasthenic crisis (20/20/20 rule)
Albuminocytologic dissociation in CSF → GBS
CK >5× ULN + myoglobinuria + hyperK + hypoCa + hyperphosphatemia + elevated uric acid → Rhabdomyolysis
Markedly elevated CK + leukocytosis + transaminitis with rigidity/fever → NMS
Reduced CMAP amplitudes with preserved sensory + clinical tick discovery → Tick paralysis
Low red-cell & plasma cholinesterase activity → Organophosphate exposure
Anti-GQ1b antibody → Miller Fisher / Bickerstaff; Anti-GT1a → Pharyngeal-cervical-brachial GBS

Treatment pearls

IVIG or PLEX (NOT both, NOT steroids) → GBS
IVIG or PLEX equally effective → Myasthenic crisis (steroids OK, often started after PLEX/IVIG begins)
Equine antitoxin (adults), BabyBIG (infants) → Botulism
Stop neuroleptic + cooling + IVF + DANTROLENE + BROMOCRIPTINE → NMS
Stop offending drug + CYPROHEPTADINE + benzodiazepines → Serotonin syndrome
DANTROLENE + active cooling + stop volatile anesthetic → Malignant hyperthermia
ATROPINE + PRALIDOXIME (2-PAM); watch for intermediate syndrome & OPIDN → Organophosphate poisoning
Aggressive IVF (UO >200–300 mL/hr); urinary alkalinization controversial → Rhabdomyolysis
Find and remove the tick → Tick paralysis; early aggressive triple immunosuppression → Anti-MDA5 RP-ILD

Guillain-Barré Syndrome (GBS)

GBS Subtypes

Subtype	Antibody	Pathology	NCS Pattern	Prognosis
AIDP	None consistently identified	Macrophage-mediated segmental demyelination	Prolonged distal latencies, slow CV, prolonged/absent F-waves, conduction block, temporal dispersion	Good; ~80% walk independently at 6 mo
AMAN	Anti-GM1, anti-GD1a	Antibody + complement attack at nodes of Ranvier → axonal degeneration (motor only)	Low CMAPs, normal SNAPs, normal CV & distal latencies; may show transient conduction block / prolonged latencies in first days (reversible conduction failure) before classic axonal pattern emerges	Variable; rapid recovery if reversible conduction failure; poor if severe axonal loss
AMSAN	Anti-GM1, anti-GD1a	Motor + sensory axonal degeneration	Low CMAPs AND low SNAPs, normal CV	Poor; prolonged recovery, severe residual deficits
Miller Fisher syndrome	Anti-GQ1b (>90%)	Cranial nerve & dorsal root ganglia involvement	Reduced/absent sensory potentials; motor studies often normal	Excellent; self-limited over weeks
Bickerstaff brainstem encephalitis	Anti-GQ1b	Brainstem inflammation + overlap with Fisher	Variable; may show CNS abnormalities on MRI	Good with treatment; altered consciousness distinguishes from Fisher
Pharyngeal-cervical-brachial	Anti-GT1a (most specific); also anti-GQ1b cross-reactivity	Oropharyngeal + neck + arm weakness (descending pattern)	Abnormal in upper limb + cranial nerves; legs spared	Generally good; may be confused with botulism

Diagnostic Workup

Test	Findings	Timing / Notes
CSF	Albuminocytologic dissociation: elevated protein (>0.45 g/L) with <10 WBC/μL	May be normal in first week; if >50 cells → consider HIV, Lyme, CMV, sarcoid, leptomeningeal disease
NCS/EMG (early)	Prolonged/absent F-waves (earliest finding); prolonged distal motor latencies; sural sparing pattern	First 1–2 weeks; may be normal day 1–3
NCS/EMG (late)	Conduction block, temporal dispersion (AIDP); low CMAPs (AMAN/AMSAN); fibrillations at 2–4 weeks if axonal	Repeat at 2–3 weeks if initial study equivocal
MRI spine	Enhancing nerve roots (especially cauda equina) on post-contrast T1	Supports diagnosis; helps exclude myelopathy
Antibodies	Anti-GQ1b (Fisher/Bickerstaff); anti-GM1/GD1a (AMAN)	Not required for diagnosis; useful for subtype classification

🎯 Clinical Pearl

Sural sparing pattern: sural sensory nerve is normal but median/ulnar sensory nerves are abnormal — highly specific for GBS (AIDP); reflects distal-predominant demyelination affecting longer nerve trunks
F-wave abnormalities (absent or prolonged) are often the earliest NCS finding because proximal nerve roots are affected first

Treatment

Therapy	Regimen	Notes
IVIg	0.4 g/kg/day × 5 days (total 2 g/kg)	Equally effective as PLEX; easier to administer; risk: aseptic meningitis, renal failure, thrombosis
PLEX	5 exchanges over ~10–14 days	Most effective if started within 7 days; requires central line; risk: hemodynamic instability, line infection
Steroids	—	NOT effective in GBS — do not use; may actually delay recovery
IVIg + PLEX	—	Do NOT combine — IVIg after PLEX just gets removed; no added benefit

Respiratory Monitoring & ICU Management

FVC every 4–6 hours — single most important bedside test
Intubation criteria (GBS 20/30/40 rule): FVC <20 mL/kg, NIF less negative than −30 cmH₂O, MEP <40 cmH₂O, >30% decline in FVC from baseline, or inability to protect airway — note: distinct from the MG 20/20/20 rule (FVC <20, NIF <−20, PaCO₂ >50)
Autonomic dysfunction: sinus tachycardia (most common), bradycardia (may require pacing), BP lability, ileus, urinary retention — continuous telemetry required
VTE prophylaxis: immobilized patients require LMWH or UFH
Pain management: neuropathic pain is common (gabapentin, pregabalin); opiate-sparing approach preferred

Prognostic Factors

Poor Prognosis	Good Prognosis
Age >60 years	Young age
Rapid onset (<7 days to nadir)	Slow progression
Need for mechanical ventilation	Preserved walking
Preceding Campylobacter jejuni diarrhea	No need for mechanical ventilation
AMAN/AMSAN subtype with severe axonal loss	AIDP with demyelinating pattern
Low distal CMAP amplitude (<20% of LLN)	Preserved CMAP amplitudes

Hughes GBS Disability Scale

Grade	Description
0	Normal
1	Minor symptoms, able to run
2	Walks ≥10 m without assistance but unable to run
3	Walks ≥10 m with assistance (walker/cane)
4	Bed- or chair-bound
5	Requires mechanical ventilation
6	Dead

Treatment-Related Fluctuations (TRF) vs Acute-Onset CIDP (A-CIDP)

Feature	Treatment-Related Fluctuation (TRF)	Acute-Onset CIDP (A-CIDP)
Frequency	~10% of treated GBS patients	~5% of patients initially diagnosed with GBS
Timing	Re-worsening within 8 weeks of treatment after initial improvement or stabilization	Deterioration >8 weeks after onset, OR ≥3 deteriorations in the course
Pathophysiology	Ongoing immune-mediated injury outlasts effect of single IVIg/PLEX course	Chronic demyelinating polyneuropathy presenting with an acute onset (mimics GBS)
Treatment	Repeat IVIg or PLEX (same course); patients usually re-respond	Start chronic immunotherapy (maintenance IVIg, steroids, or steroid-sparing agents) — steroids ARE effective in A-CIDP (unlike GBS)
Clinical clue	Single re-worsening episode ≤8 weeks; otherwise typical GBS course	Multiple relapses or late deterioration; revisit diagnosis

💎 Board Pearl

Anti-GQ1b = Miller Fisher triad (ophthalmoplegia + ataxia + areflexia); same antibody in Bickerstaff brainstem encephalitis (add altered consciousness)
AMAN is the most common subtype in Asia and post-Campylobacter — axonal, may have reversible conduction failure mimicking demyelination early on
Steroids do NOT work in GBS — one of the few autoimmune diseases where steroids are ineffective; this is a classic board question
CSF pleocytosis >50 cells in suspected GBS → reconsider diagnosis: HIV polyradiculopathy, Lyme, CMV, sarcoidosis, leptomeningeal carcinomatosis
Re-worsening after initial improvement? Within 8 weeks → TRF (repeat IVIg/PLEX); >8 weeks or ≥3 deteriorations → A-CIDP (start chronic immunotherapy)

Myasthenic Crisis

Definition & Epidemiology

Definition: MG exacerbation with respiratory failure requiring mechanical ventilation or noninvasive ventilation to avoid intubation
Occurs in ~15–20% of MG patients at some point; mortality 3–5% in modern era
Most common in first 2 years after diagnosis; AChR-positive generalized MG and MuSK-MG at highest risk

Triggers

Category	Examples
Infection	#1 trigger; URI, UTI, pneumonia, sepsis — any febrile illness can worsen transmission
Surgery	Thymectomy, any general anesthesia; avoid long-acting NMB agents (use cisatracurium)
Medications	See avoidance table below; most common offenders are antibiotics and cardiac drugs
Pregnancy/postpartum	Exacerbation often in 1st trimester and postpartum; magnesium sulfate for preeclampsia is dangerous
Immunotherapy changes	Rapid steroid taper; starting high-dose steroids acutely (transient worsening in ~50%)
Emotional/physical stress	Sleep deprivation, extreme temperatures, overexertion

Medications to Avoid in MG

Drug Class	Specific Agents	Mechanism / Risk
Aminoglycosides	Gentamicin, tobramycin, amikacin	Block presynaptic Ca²⁺ channels + postsynaptic AChR; most dangerous antibiotics in MG
Fluoroquinolones	Ciprofloxacin, levofloxacin, moxifloxacin	Pre- and postsynaptic NMJ blockade; FDA black box warning for MG
Macrolides	Azithromycin, erythromycin, clarithromycin	NMJ blockade; less dangerous than aminoglycosides but still risky
Telithromycin	Ketek	Absolutely contraindicated — fatal MG exacerbations reported; FDA contraindication
Beta-blockers	Propranolol, atenolol, metoprolol	Impair NMJ transmission; may unmask or worsen MG
Calcium channel blockers	Verapamil, diltiazem	Reduce presynaptic Ca²⁺ entry → decreased ACh release
Magnesium sulfate	IV magnesium (for pre-eclampsia, arrhythmia)	Competes with Ca²⁺ at presynaptic terminal; can precipitate crisis
D-Penicillamine	—	Can induce de novo autoimmune MG (with AChR antibodies); resolves after drug withdrawal
Immune checkpoint inhibitors	Nivolumab, pembrolizumab, ipilimumab	Can trigger fulminant MG (often with myositis + myocarditis); high mortality; may be de novo or flare of subclinical MG
Botulinum toxin	All serotypes	Can cause systemic weakness; relative contraindication
Statins	Atorvastatin, rosuvastatin	Relative risk; case reports of MG unmasking/worsening; use with caution

Management Algorithm

Step 1 — ABCs: secure airway; ICU admission; continuous respiratory monitoring (FVC and NIF every 2–4 hrs)
Step 2 — Intubation criteria (20/20/20 rule): FVC <20 mL/kg, NIF <−20 cmH₂O, PaCO₂ >50 mmHg → intubate; also intubate for rapidly declining FVC or inability to handle secretions
Step 3 — Rapid immunotherapy: IVIg (0.4 g/kg × 5 days) OR PLEX (5 exchanges); equally effective; PLEX may have faster onset; do NOT combine
Step 4 — Identify and treat trigger: cultures, imaging; start appropriate antibiotics (avoid dangerous ones); discontinue offending medications
Step 5 — Hold or reduce pyridostigmine in intubated patients (excess secretions, risk of cholinergic crisis)
Step 6 — Adjust long-term immunotherapy: start/increase corticosteroids cautiously (only after stabilized, not acutely); consider steroid-sparing agent

Cholinergic Crisis vs Myasthenic Crisis

Feature	Myasthenic Crisis	Cholinergic Crisis
Cause	Undertreated MG / disease flare	Excessive pyridostigmine / AChEi overdose
Pupils	Normal (may be mydriatic from stress)	Miotic (constricted)
Secretions	Normal	Excessive (bronchorrhea, salivation, lacrimation)
Fasciculations	Absent	Present
GI symptoms	Absent	Diarrhea, cramping, nausea
Bradycardia	Uncommon	Common (muscarinic excess)
Response to edrophonium	Improvement	Worsening
Management	IVIg or PLEX; increase immunotherapy	Stop AChEi; atropine for muscarinic symptoms; supportive care

💎 Board Pearl

Telithromycin is ABSOLUTELY contraindicated in MG — fatal crises reported; only antibiotic with an FDA contraindication specifically for MG
Do NOT start high-dose steroids acutely in myasthenic crisis — steroids can transiently worsen MG in ~50% of patients; stabilize with IVIg/PLEX first, then start steroids at low dose and titrate up
Immune checkpoint inhibitor-associated MG is a growing cause of crisis — often presents with myasthenia + myositis + myocarditis triad; check CK and troponin; high mortality
Cholinergic crisis is now rare in clinical practice (lower pyridostigmine doses used); when in doubt, stop AChEi, intubate, and reassess

Rhabdomyolysis

Definition & Pathophysiology

Definition: skeletal muscle breakdown → release of intracellular contents (CK, myoglobin, K⁺, phosphate, LDH, AST, uric acid) into circulation
Myoglobin: filtered by kidneys → precipitates in renal tubules (especially in acidic urine) → AKI via direct tubular toxicity, tubular obstruction, and vasoconstriction
CK threshold: >5× ULN (~1,000 U/L); clinically significant rhabdomyolysis often >10,000; AKI risk increases dramatically when CK >15,000–20,000

Causes

Category	Examples
Trauma / crush injury	Earthquake, prolonged immobilization, compartment syndrome, positional compression
Drugs / toxins	Statins (especially + fibrates/CYP3A4 inhibitors), alcohol, cocaine, amphetamines, heroin, NMS (antipsychotics), malignant hyperthermia (inhaled anesthetics + succinylcholine)
Metabolic / electrolyte	Hypokalemia, hypophosphatemia, hypo/hypernatremia, DKA, hypothyroidism (severe), heat stroke
Genetic metabolic myopathy	McArdle disease (myophosphorylase deficiency — glycogen storage V), CPT II deficiency (most common metabolic cause of recurrent rhabdo in adults), mitochondrial myopathies
Exercise	Extreme exertion, eccentric exercise, untrained individuals; exertional rhabdo in military/CrossFit
Seizures	Prolonged generalized tonic-clonic seizures / status epilepticus
Infections	Influenza (most common viral cause), HIV, Legionella, Streptococcus (necrotizing fasciitis)
Inflammatory myopathy	Immune-mediated necrotizing myopathy (anti-HMGCR, anti-SRP) — can cause severe CK elevation

Clinical Features & Diagnosis

Classic triad: muscle pain + weakness + dark urine (myoglobinuria) — present in <10% of cases
CK: peaks at 24–72 hrs; half-life ~36 hrs; CK >100,000 = high AKI risk
Urine: dipstick positive for "blood" (detects myoglobin) but no RBCs on microscopy — classic board finding
Electrolytes: hyperkalemia (early, dangerous), hyperphosphatemia, hypocalcemia (early — do NOT correct unless symptomatic; can rebound to hypercalcemia in recovery), hyperuricemia
DIC: tissue factor release from damaged muscle; check fibrinogen, D-dimer, PT/INR

Complications

Complication	Mechanism	Management
AKI	Myoglobin tubular obstruction + direct toxicity + renal vasoconstriction	Aggressive IV NS; renal replacement therapy if refractory
Hyperkalemia	K⁺ release from damaged muscle; worsened by AKI	Continuous cardiac monitoring; calcium gluconate, insulin/glucose, kayexalate, dialysis
Compartment syndrome	Muscle edema → increased pressure in fascial compartment → ischemia	Emergent fasciotomy; measure compartment pressures if clinical suspicion
DIC	Release of procoagulant factors from necrotic muscle	Treat underlying cause; blood products as needed
Hypocalcemia	Calcium deposition in damaged muscle; hyperphosphatemia → Ca×P precipitation	Only treat if symptomatic (seizures, arrhythmia); avoid aggressive replacement (rebound hypercalcemia)

Treatment

Aggressive IV normal saline: 200–300 mL/hr (up to 1–1.5 L/hr initially if severely volume depleted); target UO >200–300 mL/hr (or 3 mL/kg/hr)
Avoid lactated Ringer: contains K⁺ (4 mEq/L) — worsens hyperkalemia
Sodium bicarbonate: controversial; may alkalinize urine and reduce myoglobin cast formation; consider if urine pH <6.5; target urine pH >6.5; avoid if hypocalcemia present (worsens it)
Mannitol: osmotic diuresis to maintain UO; limited evidence; avoid in anuric AKI
Renal replacement therapy: for refractory AKI, severe hyperkalemia, fluid overload, metabolic acidosis
Monitor electrolytes: K⁺, Ca²⁺, phosphate, uric acid every 6–8 hrs until trending down

🎯 Clinical Pearl

When to suspect metabolic myopathy: recurrent rhabdomyolysis + young patient + exercise or fasting trigger + family history; check acylcarnitine profile, urine organic acids, ischemic forearm exercise test, genetic testing
McArdle disease: exercise intolerance, "second wind" phenomenon, myophosphorylase absent on muscle biopsy; forearm exercise test shows no rise in lactate with normal ammonia rise
CPT II deficiency: most common cause of recurrent rhabdomyolysis in young adults; triggered by prolonged exercise, fasting, cold, illness; acylcarnitine profile shows long-chain species

💎 Board Pearl

Urine dipstick positive for blood + no RBCs on microscopy = myoglobinuria — classic board answer; dipstick cannot distinguish hemoglobin from myoglobin
Do NOT aggressively correct hypocalcemia in rhabdomyolysis — calcium deposits in damaged muscle; will rebound to HYPERcalcemia during recovery phase
NMS vs malignant hyperthermia: NMS = dopamine blockers + days onset + lead-pipe rigidity; MH = inhaled anesthetics + succinylcholine + minutes onset + treat with dantrolene

Critical Illness Neuromyopathy (CINM)

CIP vs CIM Comparison

Feature	CIP (Critical Illness Polyneuropathy)	CIM (Critical Illness Myopathy)
Pathology	Axonal sensorimotor polyneuropathy (distal axonal degeneration)	Thick filament (myosin) loss; type II fiber atrophy; may have necrosis
Primary risk factors	Sepsis, SIRS, multi-organ failure	Corticosteroids + neuromuscular blocking agents (vecuronium, rocuronium)
Motor NCS	Low CMAPs, normal CV (axonal pattern)	Low CMAPs, normal CV (myopathic); short-duration MUPs
Sensory NCS	Reduced/absent SNAPs (key distinguishing feature)	Normal SNAPs
EMG needle exam	Fibrillation potentials; long-duration, high-amplitude MUPs with reduced recruitment (neurogenic)	Fibrillation potentials; short-duration, low-amplitude MUPs with early recruitment (myopathic)
Direct muscle stimulation	CMAP/direct muscle stimulation ratio preserved (>0.5)	CMAP/direct muscle stimulation ratio reduced (<0.5) — muscle itself inexcitable
CK	Normal or mildly elevated	May be elevated (but often normal — unreliable)
Biopsy	Axonal degeneration (nerve)	Myosin/thick filament loss (muscle) — pathognomonic
Prognosis	Worse; slow recovery over months to years; residual deficits common	Better; most recover over weeks to months
Overlap (CIPNM)	Most ICU patients have combined CIP + CIM; pure forms are less common. The CIP-vs-CIM dichotomy is a simplification — overlap and shared risk factors (sepsis, steroids, NMB agents, hyperglycemia, immobility) are common in practice

Clinical Presentation

Failure to wean from ventilator + flaccid quadriparesis — hallmark presentation
Diffuse, symmetric limb weakness (proximal ≥ distal); facial muscles often spared
Hyporeflexia or areflexia
Sensation difficult to assess in sedated patients; CIP may have distal sensory loss
Typically develops after ≥1 week in ICU

Differential Diagnosis of ICU Weakness

Diagnosis	Key Distinguishing Feature
CINM	Diffuse weakness after prolonged ICU stay; sepsis/steroids/NMB agents; NCS abnormalities
Prolonged NMB effect	Recent NMB agent use; resolves within hours to days; normal NCS once NMB cleared; train-of-four monitoring
GBS (ICU-acquired)	Ascending pattern; albuminocytologic dissociation; demyelinating NCS; enhancing nerve roots on MRI
Cervical myelopathy	UMN signs (hyperreflexia, Babinski); sensory level; MRI spine diagnostic
Undiagnosed MG	Fatigable weakness; RNS shows decrement; positive AChR/MuSK Ab

Risk Factors & Prevention

Risk Factor	Prevention Strategy
Sepsis / SIRS / multi-organ failure	Early source control; appropriate antibiotics
Corticosteroids (especially high-dose IV)	Minimize dose and duration; taper as soon as possible
Neuromuscular blocking agents	Limit use; daily sedation holidays; monitor train-of-four
Hyperglycemia	Strict glycemic control (target <180 mg/dL; avoid hypoglycemia)
Prolonged immobility	Early mobilization (strongest evidence for prevention)
Prolonged mechanical ventilation	Minimize sedation; daily spontaneous breathing trials

💎 Board Pearl

Normal SNAPs = CIM; reduced SNAPs = CIP — the single most important electrodiagnostic distinction (sensory nerves are not affected by myopathy)
Direct muscle stimulation can distinguish CIM from CIP even in uncooperative patients — if muscle is directly inexcitable, it is CIM
CIM has better prognosis than CIP — muscle regeneration is faster than axonal regrowth
Early mobilization is the only intervention with strong evidence to prevent CINM — no specific pharmacologic treatment exists

Acute Flaccid Paralysis — Differential Diagnosis

Master DDx Table

Diagnosis	Onset	Distribution	Reflexes	Sensory	Respiratory	Pupils	Key Test	Treatment
GBS (AIDP)	Days (ascending over 1–4 wk)	Symmetric, ascending; proximal & distal	Areflexia	Paresthesias, pain; mild sensory loss	30% need ventilation	Normal	CSF (albuminocytologic dissociation); NCS (demyelinating)	IVIg or PLEX
Myasthenic crisis	Hours to days	Bulbar + respiratory; proximal limbs; fatigable	Normal	Normal	Prominent (crisis definition)	Normal	AChR/MuSK Ab; RNS (decrement); FVC	IVIg or PLEX; treat trigger
CINM	Days to weeks (after ICU)	Diffuse, symmetric; failure to wean	Reduced / absent	Difficult to assess; may have distal loss (CIP)	Failure to wean	Normal	NCS/EMG; direct muscle stimulation	Supportive; early mobilization
Botulism	Hours to days (descending)	Descending: cranial nerves → arms → legs	Reduced / absent	Normal	Yes (may need prolonged ventilation)	Dilated, fixed	Stool toxin assay; NCS (low CMAP + facilitation)	Antitoxin; supportive
Tick paralysis	Days (ascending over 1–5 days)	Symmetric, ascending (mimics GBS)	Areflexia	Normal (usually)	Yes (if untreated)	Normal (may have dilated)	Find and remove tick; normal CSF; normal NCS early	Tick removal → rapid improvement (hours)
Periodic paralysis	Minutes to hours (episodic)	Symmetric, proximal; spares respiratory and cranial	Reduced during attack	Normal	Rare	Normal	K⁺ level (hypo or hyper); genetic testing	Correct K⁺; acetazolamide (prevention)
Transverse myelitis	Hours to days	Bilateral (often asymmetric); below lesion level	Initially flaccid (spinal shock) → later hyperreflexic	Sensory level	If cervical	Normal	MRI spine (T2 lesion); CSF (pleocytosis)	IV methylprednisolone; PLEX if refractory
AFM (acute flaccid myelitis)	Days (often after febrile illness)	Asymmetric limb weakness; children	Reduced / absent in affected limbs	Minimal	May need ventilation	Normal	MRI (spinal cord gray matter T2 lesion); enterovirus D68/A71 PCR	Supportive; IVIg (limited evidence); no proven therapy

🎯 Clinical Pearl

Tick paralysis mimics GBS almost perfectly (ascending paralysis + areflexia + normal CSF) — always examine the scalp and hair for an engorged tick; removal leads to dramatic improvement within hours
Transverse myelitis initially causes flaccid paralysis (spinal shock) that can be confused with GBS — sensory level and bladder dysfunction are key differentiators; reflexes become hyperactive later
AFM: think of it in a child with acute asymmetric limb weakness after a viral illness; MRI shows gray matter lesion in the spinal cord (anterior horn cells); enterovirus D68 is the most commonly associated pathogen

💎 Board Pearl

Ascending paralysis = GBS or tick paralysis; descending paralysis = botulism or pharyngeal-cervical-brachial GBS variant
Dilated unreactive pupils = botulism (NOT GBS, NOT MG) — the single best bedside clue
Normal CSF + normal NCS + ascending paralysis that resolves after tick removal = tick paralysis
Spinal shock (flaccid + areflexic) from acute myelopathy is the great mimicker of GBS on initial exam — check for sensory level and Babinski sign

Respiratory Failure in Neuromuscular Disease

Causes

Condition	Mechanism of Respiratory Failure	Key Feature
Myasthenic crisis	Diaphragm & intercostal NMJ transmission failure	Fatigable; may improve with rest then worsen again
GBS	Phrenic nerve + intercostal nerve demyelination/axonal injury	Progressive ascending; monitor FVC trend
ALS	Motor neuron degeneration → diaphragm denervation; bulbar weakness → aspiration	Insidious; orthopnea early sign; FVC <50% → consider NIV
High cervical cord injury (C3–C5)	Phrenic motor neurons (C3–C5) damaged → diaphragm paralysis	Acute onset; C3–C5 “keeps the diaphragm alive”
Phrenic neuropathy	Bilateral phrenic nerve injury (post-cardiac surgery, neuralgic amyotrophy, ICU)	Orthopnea; paradoxical abdominal motion; sniff test positive
Acid maltase deficiency (Pompe disease)	Glycogen accumulation in diaphragm → early respiratory failure disproportionate to limb weakness	Adult-onset: respiratory failure may be presenting symptom; check acid alpha-glucosidase level

Respiratory Monitoring

Parameter	Normal	Concerning	Critical / Intubate
FVC (best single test)	>60 mL/kg	<30 mL/kg	<20 mL/kg or >30% decline
NIF (MIP)	More negative than −60 cmH₂O	Less negative than −30 cmH₂O	Less negative than −20 cmH₂O
PaCO₂	35–45 mmHg	>45 mmHg	>50 mmHg (hypoventilation)
SpO₂	>95%	<92%	Late finding — hypoxemia occurs only after severe hypoventilation; do NOT rely on SpO₂ alone

Diaphragm Assessment

Test	Method	Findings in Diaphragm Weakness
Sniff test (fluoroscopy)	Observe diaphragm movement during quick sniff	Paradoxical upward motion of hemidiaphragm during sniff
Phrenic nerve conduction	Stimulate phrenic nerve at neck; record diaphragm CMAP	Prolonged latency (demyelination) or low/absent CMAP (axonal)
Diaphragm ultrasound	Measure diaphragm thickness and thickening ratio during inspiration	Thickening ratio <20% (normal >20%); reduced excursion; increasingly used bedside in ICU
Supine vs upright FVC	Measure FVC sitting then supine	>20% drop in supine position suggests diaphragm weakness (abdominal contents push up against weak diaphragm)

When FVC May Be Misleading

Bulbar weakness: poor lip seal around mouthpiece → falsely low FVC; use face mask
Facial weakness: air leak around mouthpiece → underestimates true FVC
Uncooperative / sedated patient: effort-dependent test; unreliable results
Supplemental O₂: may mask hypoventilation by maintaining SpO₂; always check PaCO₂

NIV vs Invasive Ventilation

Feature	NIV (BiPAP)	Invasive (Intubation)
Indications	Chronic progressive NM disease (ALS, DMD); nocturnal hypoventilation; FVC 20–50% predicted	Acute crisis (GBS, MG crisis); FVC <20 mL/kg; inability to protect airway; copious secretions
Contraindications to NIV	Bulbar dysfunction with aspiration risk; inability to clear secretions; hemodynamic instability; altered consciousness	—
ALS-specific	Start NIV when FVC <50% predicted or symptomatic orthopnea/sleep-disordered breathing; prolongs survival 7–13 months	Tracheostomy if patient elects long-term ventilation; discuss goals of care early

💎 Board Pearl

FVC is the best single bedside test for neuromuscular respiratory failure, but clinical trajectory and ability to protect the airway are more important than any single FVC value. Intubate based on the gestalt — rate of decline, bulbar dysfunction, secretion handling, work of breathing — not just the number. SpO₂ drops late and PaCO₂ rises late; by the time they are abnormal, the patient is already in trouble.
Supine FVC drop >20% = diaphragm weakness; this is often the earliest sign of respiratory compromise in NM disease (before upright FVC falls)
Pompe disease (acid maltase deficiency) causes respiratory failure OUT OF PROPORTION to limb weakness — diaphragm is preferentially affected; always check in unexplained respiratory failure + proximal myopathy
“C3, 4, 5 keeps the diaphragm alive” — injuries at or above C3–C5 paralyze the diaphragm via phrenic nerve

Toxin-Related Neuromuscular Emergencies

Comparison of NM Toxins

Toxin / Agent	Mechanism	Clinical Presentation	Pupils	Key Treatment
Botulinum toxin	Cleaves SNARE proteins → blocks presynaptic ACh vesicle release	Descending paralysis: cranial nerves → arms → legs; dry mouth; constipation; alert mental status. RNS: post-exercise facilitation / incremental response on high-frequency (20–50 Hz) RNS — analogous to LEMS pattern	Dilated, unreactive	Foodborne/adult: equine heptavalent antitoxin (BAT); Wound botulism: heptavalent antitoxin + antibiotics (penicillin G or metronidazole) + surgical debridement; Infant botulism: BabyBIG only — AVOID aminoglycosides (potentiate paralysis via presynaptic Ca²⁺ blockade) and AVOID empiric antibiotics (lysis of organisms releases additional toxin); NO anticholinesterases (presynaptic block — no ACh to preserve); supportive care; may need prolonged ventilation
Organophosphate / nerve agent	Irreversibly inhibits AChE → excess ACh at muscarinic AND nicotinic receptors	Muscarinic (SLUDGE): salivation, lacrimation, urination, diarrhea/diaphoresis, GI cramping, emesis; + bradycardia, bronchospasm, bronchorrhea Nicotinic: fasciculations, weakness, paralysis, tachycardia CNS: seizures, coma	Miotic (constricted)	Atropine (muscarinic blockade; titrate to dry secretions); pralidoxime (2-PAM) (reactivates AChE if given before “aging”); benzodiazepines for seizures; decontamination
Black widow spider (latrotoxin)	α-Latrotoxin → massive presynaptic ACh (and catecholamine) release → vesicle depletion	Severe pain at bite site → diffuse muscle spasms (especially abdominal rigidity mimicking acute abdomen); diaphoresis; HTN; tachycardia	Normal	IV calcium gluconate or opioids for pain/spasm; antivenin (Latrodectus) for severe cases; benzodiazepines
Tetrodotoxin (puffer fish)	Blocks voltage-gated Na⁺ channels on nerve and muscle membranes → prevents AP generation	Perioral paresthesias (onset 10–45 min after ingestion) → ascending paralysis → respiratory failure; alert mental status; GI symptoms	Fixed, dilated (late)	Supportive care ONLY — no antidote; mechanical ventilation as needed; full recovery if survive initial 24 hrs
Tetanus (Clostridium tetani)	Tetanospasmin blocks inhibitory interneurons (glycine + GABA release) in spinal cord → unopposed motor neuron firing	Trismus (lockjaw) → risus sardonicus → opisthotonus → generalized muscle spasms; autonomic instability; mental status preserved	Normal	Human tetanus immunoglobulin (TIG); metronidazole; benzodiazepines (spasm control); magnesium sulfate (controls autonomic instability and spasms); intrathecal baclofen for refractory spasms; wound debridement; ICU for autonomic instability
Tick paralysis	Salivary neurotoxin blocks presynaptic ACh release at NMJ (and possibly Na⁺ channels)	Ascending flaccid paralysis over 1–5 days; ataxia; areflexia; mimics GBS closely	Normal (may dilate late)	Tick removal → rapid improvement within hours; no other specific therapy; search scalp thoroughly

Organophosphate Poisoning — SLUDGE & Beyond

SLUDGE (muscarinic): Salivation, Lacrimation, Urination, Diarrhea/Diaphoresis, GI cramping, Emesis
“Killer Bs” (muscarinic): Bradycardia, Bronchospasm, Bronchorrhea — cause of death if untreated
Nicotinic effects: fasciculations, muscle weakness, paralysis (may need ventilation), tachycardia, mydriasis (competes with miosis)
CNS: anxiety, seizures, coma, respiratory center depression
Intermediate syndrome: proximal weakness + cranial nerve palsies + respiratory failure 24–96 hrs after initial cholinergic crisis resolves; thought to be due to persistent NMJ dysfunction
OPIDN (organophosphate-induced delayed neuropathy): distal axonopathy 2–4 weeks after exposure; sensorimotor polyneuropathy; inhibition of neuropathy target esterase (NTE)

Botulism vs Organophosphate — Quick Comparison

Feature	Botulism	Organophosphate
Mechanism	Blocks ACh release (too little ACh)	Blocks AChE (too much ACh)
Pupils	Dilated (mydriasis)	Constricted (miosis)
Secretions	Dry (decreased ACh)	Excessive (SLUDGE)
Fasciculations	Absent	Present
Paralysis pattern	Descending	Generalized (nicotinic phase)
Heart rate	Normal or tachycardic	Bradycardic (muscarinic) or tachycardic (nicotinic)
Antidote	Antitoxin	Atropine + pralidoxime (2-PAM)

💎 Board Pearl

Anticholinesterases are USELESS in botulism — there is no ACh being released to preserve; the block is presynaptic (SNARE protein cleavage prevents vesicle fusion entirely)
Pralidoxime (2-PAM) must be given early — once organophosphate “ages” (irreversible AChE binding, typically 24–48 hrs), 2-PAM cannot reactivate the enzyme
Organophosphate intermediate syndrome (24–96 hrs post-exposure): proximal weakness + respiratory failure AFTER cholinergic crisis resolves — not prevented by atropine or 2-PAM; requires ventilatory support
OPIDN (delayed neuropathy) occurs 2–4 weeks after exposure and causes a distal sensorimotor axonopathy — distinct from acute cholinergic effects
Tetanus is NOT a flaccid paralysis — it causes rigid/spastic paralysis (blocks inhibitory interneurons); do not confuse with botulism (flaccid, blocks ACh release)

Periodic Paralyses

Overview

Channelopathies of skeletal muscle causing episodic, symmetric, proximal-predominant weakness; respiratory and cranial muscles typically spared
Reflexes are reduced or absent during attacks, normal between attacks
Categorized by serum K⁺ during attack: hypokalemic, hyperkalemic, or normokalemic; thyrotoxic periodic paralysis is an acquired form of HypoKPP

Comparison of Periodic Paralysis Subtypes

Feature	Hypokalemic PP (HypoKPP)	Thyrotoxic PP (TPP)	Hyperkalemic PP (HyperKPP)
Gene / Channel	CACNA1S (Ca_v1.1, most common) or SCN4A (Na_v1.4); autosomal dominant	Acquired; KCNJ18 (Kir2.6) variants in some patients; associated with thyrotoxicosis	SCN4A (Na_v1.4); autosomal dominant
Demographics	Onset adolescence; M>F	Asian males 20–40 yrs; underlying hyperthyroidism (Graves')	Onset childhood; equal sex distribution
Triggers	High-carbohydrate meal, rest after exercise, alcohol, stress, cold	Carbohydrate load, exercise, stress; often nocturnal	Rest after exercise, fasting, K⁺-rich foods, cold, stress
Attack duration	Hours to days	Hours to ~36 hrs	Minutes to hours (shorter)
Serum K⁺ in attack	Low (often <3.0)	Low	High or high-normal
Myotonia	Absent	Absent	Often present (paramyotonia congenita overlap)
Acute treatment	Oral KCl (preferred); IV KCl in dextrose-free saline if severe (dextrose worsens by driving K⁺ intracellular)	K⁺ replacement + non-selective beta-blocker (propranolol) + treat hyperthyroidism (methimazole/PTU, definitive thyroid therapy)	Carbohydrate load, mild exercise, IV calcium gluconate, inhaled beta-agonist (albuterol), IV glucose+insulin
Prevention	Low-carb, low-Na diet; acetazolamide or dichlorphenamide; K⁺-sparing diuretics	Definitive treatment of hyperthyroidism (curative)	Avoid triggers; thiazides; acetazolamide or dichlorphenamide
EMG (between attacks)	Long exercise test: post-exercise CMAP decrement	Long exercise test: post-exercise CMAP decrement	Often myotonic discharges; cold-induced changes

🎯 Clinical Pearl

TPP red flags: Asian male, 20–40, nocturnal/post-carbohydrate proximal weakness with low K⁺ — always check TSH/free T4; treating the thyroid is curative
Use propranolol (non-selective beta-blocker) in TPP — blunts beta-adrenergic-driven intracellular K⁺ shift and treats thyrotoxic symptoms
Andersen-Tawil syndrome (KCNJ2) is a distinct channelopathy — triad of periodic paralysis (variable K⁺) + long-QT/ventricular arrhythmia + dysmorphic features (low-set ears, micrognathia, clinodactyly)

💎 Board Pearl

Thyrotoxic periodic paralysis = Asian male + hyperthyroidism + hypokalemia — treat with K⁺ + propranolol + definitive thyroid therapy
HypoKPP: avoid IV dextrose when replacing K⁺ — insulin response shifts K⁺ further intracellularly and worsens the attack
HyperKPP often has myotonia; HypoKPP and TPP do not
Respiratory and cranial muscles are spared in periodic paralysis — this is a key distinguishing feature from GBS, MG crisis, and botulism

Acute Intermittent Porphyria (AIP)

Overview

Autosomal dominant deficiency of hydroxymethylbilane synthase (porphobilinogen deaminase) — the 3rd enzyme of heme biosynthesis
Attacks precipitated by drugs (cytochrome P450 inducers: barbiturates, phenytoin, carbamazepine, sulfonamides, rifampin, sex hormones), fasting, alcohol, infection, stress, menstruation
Young women (puberty–menopause) most affected

Clinical Tetrad

Domain	Features
Severe abdominal pain	Diffuse, colicky, often without peritoneal signs; nausea, vomiting, constipation; mimics surgical abdomen
Autonomic dysfunction	Tachycardia, hypertension, sweating, urinary retention, ileus
Psychiatric / CNS	Anxiety, agitation, hallucinations, psychosis, seizures (often in setting of hyponatremia/SIADH), confusion
Motor neuropathy	Acute predominantly motor axonal neuropathy; may be proximal > distal; can mimic GBS but with prominent pain, autonomic, and psychiatric features; cranial nerve involvement possible; respiratory failure in severe cases
Hyponatremia	Common; SIADH from hypothalamic involvement; may precipitate seizures

Diagnosis

Urine porphobilinogen (PBG): markedly elevated during attack — single best test; collect spot urine during symptoms
Urine ALA (delta-aminolevulinic acid) also elevated; urine may darken on standing/light exposure (porphobilin)
Genetic testing for HMBS mutation confirms diagnosis and identifies at-risk relatives

Treatment

IV hemin (heme arginate or hematin): first-line; suppresses ALA synthase via feedback → reduces neurotoxic precursors
IV glucose / high-carbohydrate load (~300–500 g/day): suppresses ALA synthase; useful for mild attacks or while awaiting hemin
Stop all porphyrinogenic drugs; treat triggers (infection, fasting)
Symptomatic: opioids for pain, beta-blockers for tachycardia/HTN, careful Na⁺ correction for SIADH, benzodiazepines or gabapentin for seizures (avoid phenytoin, carbamazepine, barbiturates — porphyrinogenic)
Givosiran (siRNA against ALAS1) for prevention of recurrent attacks

💎 Board Pearl

AIP classic stem: young woman, severe abdominal pain + psychiatric symptoms + motor neuropathy + hyponatremia/seizures + recent exposure to a P450-inducing drug → check urine PBG, treat with IV hemin + glucose
Avoid phenytoin, carbamazepine, barbiturates, sulfonamides, rifampin — all porphyrinogenic; benzodiazepines and gabapentin are safer for AIP-related seizures
Hyponatremia in AIP = SIADH; sodium correction must be slow to avoid osmotic demyelination

Lead Poisoning (Plumbism)

Sources & Pathophysiology

Occupational (battery manufacturing, smelting, painting, ammunition), old paint/plumbing (pediatric pica), contaminated water, retained bullets, some imported cosmetics and folk remedies
Lead inhibits multiple steps of heme synthesis (ALA dehydratase, ferrochelatase) and interferes with mitochondrial function, calcium signaling, and NMDA receptors

Clinical Features

System	Findings
Peripheral nervous system (adults)	Predominantly motor axonal neuropathy; classic wrist drop (radial-predominant) and foot drop; may be asymmetric
CNS (especially children)	Encephalopathy (cerebral edema, seizures, coma), cognitive impairment, behavioral changes, developmental delay
GI	Colicky abdominal pain, constipation, anorexia, metallic taste
Hematologic	Microcytic anemia with basophilic stippling on peripheral smear
Mucosal / skeletal	Burton's lines (blue-black gingival discoloration); lead lines at metaphyses on long-bone X-ray in children
Renal	Chronic tubulointerstitial nephritis; gout (saturnine gout)

Diagnosis & Treatment

Whole blood lead level is the diagnostic test of choice; also check zinc protoporphyrin/free erythrocyte protoporphyrin, CBC with smear (microcytic anemia + basophilic stippling), basic metabolic panel, urine ALA
Remove source of exposure — cornerstone of therapy
Chelation (thresholds vary by guideline and age):
- Succimer (DMSA) — oral; outpatient chelation for moderate elevations
- CaNa₂EDTA +/− dimercaprol (BAL) — severe poisoning, encephalopathy, very high levels; dimercaprol given first in encephalopathy to avoid redistribution into CNS

💎 Board Pearl

Adult with wrist drop + basophilic stippling + microcytic anemia + gum line → lead poisoning; ask about occupation (battery, smelter, painter, gunsmith)
Predominantly MOTOR neuropathy — one of the few causes (along with porphyria, diphtheria, AMAN-GBS) to remember on boards
In lead encephalopathy, give dimercaprol (BAL) before EDTA — EDTA alone can mobilize lead and worsen CNS toxicity

Diphtheritic Polyneuropathy

Overview

Caused by Corynebacterium diphtheriae exotoxin — inhibits protein synthesis (ADP-ribosylates eEF-2) and causes segmental demyelination of peripheral nerves
Rare in vaccinated populations; consider in unvaccinated patients or outbreaks (e.g., refugee populations, former Soviet states)

Clinical Course

Phase	Timing After Initial Infection	Features
1. Local infection	Acute	Pharyngitis with adherent grayish pseudomembrane, fever, lymphadenopathy ("bull neck"); cutaneous form has indolent ulcer
2. Bulbar palsy	~1–2 weeks	Palatal weakness, nasal speech/regurgitation, dysphagia, blurred vision (accommodation paresis from ciliary involvement)
3. Descending demyelinating polyneuropathy	~2–8 weeks (up to 3 months)	Symmetric sensorimotor demyelinating neuropathy resembling GBS; respiratory muscle and limb weakness; may need ventilation
4. Cardiac	~1–6 weeks	Myocarditis with heart block, arrhythmia, heart failure — leading cause of death

Diagnosis & Treatment

Throat culture on Loeffler or tellurite medium; toxin assay (Elek test); PCR
Diphtheria antitoxin (equine) — give as soon as suspected; only neutralizes unbound toxin (urgent)
Antibiotics: erythromycin or penicillin G; eradicates organism but does not reverse toxin already bound
Supportive care: airway protection, cardiac monitoring, ICU; respiratory and cardiac complications drive mortality
Vaccinate close contacts; treat contacts with antibiotic prophylaxis

💎 Board Pearl

Pharyngitis with pseudomembrane → bulbar palsy at 1–2 weeks → demyelinating polyneuropathy at 2–8 weeks → myocarditis — classic diphtheria sequence
Accommodation paresis (blurred near vision) with preserved pupillary light reflex is a characteristic early finding (selective ciliary muscle involvement)
Antitoxin must be given empirically on clinical suspicion — do not wait for culture; antibiotics alone are inadequate because most morbidity is from already-bound toxin

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