Role of Medical Nutrition Therapy in Guillain-Barré Syndrome AMAN and Miller Fisher Variants With Sodium and Potassium Disorders: A Case Series

Guillain–Barré syndrome (GBS) is an acute immune-mediated neuropathy that may cause respiratory failure, cranial nerve palsies, and autonomic dysfunction. Malnutrition and electrolyte disturbances, particularly hyponatremia and hypokalemia, are common and can worsen prognosis. Medical nutrition therapy (MNT) is essential to optimize recovery by meeting energy, protein, and electrolyte needs. This case series reports four hospitalized GBS patients—three with acute motor axonal neuropathy (AMAN) and one with the Miller Fisher syndrome (MFS) variant—presenting with moderate protein–energy malnutrition and sodium/potassium imbalances. All had preceding upper respiratory infections, progressive tetraparesis, and dysphagia. AMAN cases were more severe (GBS disability score 4, high EGRIS), with one requiring mechanical ventilation, while the MFS patient showed ophthalmoplegia and bulbar palsy. Hyponatremia (Na 124–135 mmol/L) was found in all patients and hypokalemia in two. Individualized MNT provided 25–40 kcal/kg/day and 1.2–1.5 g protein/kg/day via oral or enteral feeding, with parenteral nutrition as needed, alongside strict electrolyte correction and micronutrient support. Nutrition interventions began within 1–4 weeks of admission. Functional and biochemical markers gradually improved. Earlier plasmapheresis (day 15) and timely MNT were associated with faster respiratory and functional recovery. This series highlights the importance of early, individualized MNT as part of multidisciplinary GBS management to enhance outcomes and reduce complications.