## Pathophysiology & Clinical Features of GBS **Key Point:** Guillain-Barré Syndrome is an acute, post-infectious, immune-mediated polyradiculoneuropathy characterized by ascending paralysis, areflexia, and demyelination on nerve conduction studies. ### Why Option 3 (Autonomic Dysfunction) is INCORRECT **High-Yield:** Autonomic dysfunction is a SIGNIFICANT and COMMON feature of GBS, not rare or clinically insignificant. It occurs in up to 65% of hospitalized GBS patients and can be life-threatening. **Clinical Pearl:** Autonomic manifestations include: - Cardiac arrhythmias (tachycardia, bradycardia, asystole) - Hypertension or hypotension - Urinary retention - Pupillary dysfunction - Facial flushing - Labile blood pressure These complications are a major reason for ICU monitoring in severe GBS and contribute significantly to morbidity and mortality. ### Correct Statements (Options 1, 2, 4) | Feature | Details | |---------|----------| | **Demyelination** | Primary mechanism in ~90% of cases (AIDP — Acute Inflammatory Demyelinating Polyradiculoneuropathy). Axonal variants (AMAN, AMSAN) occur in ~10%, especially in Asia. | | **Respiratory Failure** | Occurs in 20–30% of patients; requires mechanical ventilation. Bulbar involvement and diaphragmatic paralysis are key risk factors. | | **C. jejuni** | Most common antecedent infection worldwide (~30% of cases). Also associated with Zika, CMV, EBV, and other viral/bacterial pathogens. | **Mnemonic for GBS Triggers:** **CAMP** — *Campylobacter, Acute infection, Mycoplasma, Post-surgical/vaccination* ### Clinical Monitoring Essentials 1. **Vital capacity** — serial measurement to predict respiratory failure risk 2. **Cardiac monitoring** — continuous ECG for arrhythmia detection 3. **Blood pressure** — frequent checks given autonomic instability 4. **Plasma exchange or IVIG** — standard immunotherapy within 2 weeks of symptom onset [cite:Harrison 21e Ch 379]
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