Plasmapheresis or Intravenous Immunoglobulin (IVIg)
This patient has Guillain-Barré syndrome (GBS) with severe features (grade 3-4) including bulbar weakness (dysphagia, diplopia), and requires immediate treatment with either IVIg (0.4 g/kg/day for 5 days) or plasmapheresis, with IVIg generally preferred due to easier administration and wider availability. 1
Clinical Presentation Confirms Severe GBS
This patient presents with classic post-infectious GBS following Campylobacter jejuni enteritis, manifesting as:
- Ascending weakness progressing from legs to arms over 2 weeks 2
- Bulbar involvement with dysphagia and diplopia, indicating cranial nerve involvement 2, 1
- Hyporeflexia with distal paresthesias but intact proprioception, consistent with peripheral nerve pathology 2
- Grade 3-4 severity based on the presence of dysphagia and extraocular muscle palsies 2, 1
The PaO2 of 88 mm Hg suggests borderline respiratory function that requires close monitoring, though not yet requiring mechanical ventilation 2.
First-Line Treatment: IVIg or Plasmapheresis
IVIg is the preferred first-line treatment for this patient with severe GBS:
- Dosing: 0.4 g/kg/day for 5 consecutive days (total dose 2 g/kg) 1, 3
- Equally effective to plasmapheresis but easier to administer with higher completion rates 1, 3
- Should be initiated immediately given the severe features including dysphagia, facial weakness, and rapidly progressive symptoms 2, 1
Plasmapheresis is an equally effective alternative:
- Regimen: 5 sessions at 200-250 mL/kg 3
- Consider if IVIg unavailable or if patient has IgA deficiency (increased anaphylaxis risk with IVIg) 1
- Both treatments are equally effective, but IVIg is generally preferred for practical reasons 1, 4
Why Other Options Are Incorrect
Azithromycin has no role here—the C. jejuni infection has already resolved, and the current presentation is post-infectious autoimmune neuropathy, not active infection 4, 5.
Continuous positive airway pressure (CPAP) is premature—while respiratory monitoring is critical, the PaO2 of 88 mm Hg does not yet indicate respiratory failure requiring ventilatory support 2. However, the patient requires admission to a unit with rapid ICU transfer capability 2, 1.
Corticosteroids alone are not recommended for GBS treatment—multiple randomized controlled trials have shown no significant benefit, and oral corticosteroids may have negative effects 1, 6, 4. While pulse methylprednisolone may be considered in combination with IVIg for immune checkpoint inhibitor-related GBS, this patient has classic post-infectious GBS 2, 1.
Vitamin B12 is irrelevant—this patient has acute autoimmune polyradiculoneuropathy, not B12 deficiency neuropathy, which presents with subacute/chronic progression and different clinical features 2.
Critical Management Considerations
Immediate hospitalization with ICU-level monitoring capability is essential given:
- Bulbar weakness (dysphagia) increases aspiration risk 2, 1
- Respiratory monitoring using the "20/30/40 rule": risk of respiratory failure if vital capacity <20 mL/kg, maximum inspiratory pressure <30 cmH2O, or maximum expiratory pressure <40 cmH2O 2, 1
- Autonomic dysfunction monitoring for arrhythmias and blood pressure fluctuations 2, 3
Avoid medications that worsen neuromuscular function:
Monitor for treatment-related fluctuations (TRFs):
- Occur in 6-10% of patients within 2 months after initial improvement 1, 3
- Require repeat full course of IVIg or plasmapheresis 3, 7
Prognosis and Follow-up
Despite treatment, GBS remains serious: