Guillain-Barré syndrome and acute flaccid paralysis: SAQ

This boy presents the classic picture of Guillain-Barré syndrome: a preceding Campylobacter-like diarrhoeal illness, progressive symmetrical ascending flaccid weakness over days, and early areflexia without a sensory level. His falling forced vital capacity and bulbar weakness are the immediate threats, and they drive the decision to escalate to intensive care. The diagnosis is made on the clinical picture, and the disease-modifying treatment is intravenous immunoglobulin. ^[1]

Question 1 (10 marks)

Outline your immediate assessment, the investigations you would request, and your initial management over the first 24 hours. ^[1]

I would treat this as probable Guillain-Barré syndrome and escalate immediately to intensive care, because the forced vital capacity of 18 mL per kilogram is under the 20 mL per kilogram threshold and has fallen by more than 30 percent from baseline, and the weak cough with pooled secretions signals bulbar weakness and aspiration risk. The decision to intubate is driven by the numbers, not by how the child looks, and a child who is still talking can have a falling vital capacity. I would secure the airway, preoxygenate, and arrange a rapid sequence induction with the intensive care team, and place continuous cardiac and haemodynamic monitoring for autonomic instability. ^[12]

The workup runs in parallel. I would send the cerebrospinal fluid for cell count, protein, glucose, oligoclonal bands, and viral polymerase chain reaction including Campylobacter and enterovirus studies, knowing that albuminocytological dissociation may be absent in the first week and a normal early result does not exclude the diagnosis. I would request neurophysiology to distinguish the demyelinating AIDP from the axonal AMAN and AMSAN subtypes, and a ganglioside antibody panel including anti-GM1, anti-GD1a, and anti-GQ1b. I would obtain a spinal MRI only if any cord feature such as a sensory level, bladder or bowel dysfunction, or asymmetric weakness appeared, to exclude transverse myelitis, acute flaccid myelitis, or cord compression. ^[2]

I would start first-line therapy with intravenous immunoglobulin 2 g per kg over two to five days, which the van der Meche 1992 trial showed to be as effective as plasma exchange and which the Cochrane review confirmed speeds recovery. I would not give corticosteroids, because the systematic review showed no benefit and possible harm. I would add prophylactic anticoagulation for venous thromboembolism, pressure-area care, nasogastric nutrition for the bulbar weakness, and pain management with gabapentin or opiates, and I would involve paediatric neurology and plan retrieval to a tertiary centre. ^[4][5][7]