Guillain-Barré syndrome and acute flaccid paralysis: Case

Summary and immediate impression

This boy presents a textbook case of Guillain-Barré syndrome. The tempo is subacute over days, with a Campylobacter-like diarrhoeal illness two weeks earlier, progressive symmetrical ascending flaccid weakness, and early areflexia without a sensory level. The falling forced vital capacity and the 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]

The first 24 hours — resuscitation, monitoring, and intensive care

I would treat this as probable Guillain-Barré syndrome and escalate immediately to intensive care. 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. I would secure the airway, preoxygenate, and arrange a rapid sequence induction with the intensive care team, because the weak respiratory muscles and the risk of aspiration make this a high-risk airway. I would place continuous cardiac and haemodynamic monitoring for autonomic instability with arrhythmia and blood pressure swings. [12]

The workup runs in parallel. I send the cerebrospinal fluid for cell count, protein, glucose, oligoclonal bands, and viral studies, knowing that albuminocytological dissociation may be absent in the first week. I request neurophysiology to distinguish the demyelinating AIDP from the axonal AMAN and AMSAN subtypes, and a ganglioside antibody panel. I do not need a spinal MRI because there is no sensory level, no bladder or bowel dysfunction, and no asymmetric weakness to suggest a cord lesion or acute flaccid myelitis. I notify the public-health unit because acute flaccid paralysis in a child under fifteen years is a notifiable event that triggers stool testing for poliovirus. [2]

I start first-line therapy with intravenous immunoglobulin 2 g per kg over two to five days, giving 44 grams in total for this 22 kilogram child. I do not give corticosteroids, because the systematic review showed no benefit and possible harm. I add prophylactic anticoagulation for venous thromboembolism, pressure-area care, nasogastric nutrition for the bulbar weakness, and pain management with gabapentin, and I involve paediatric neurology and plan retrieval to a tertiary centre if not already there. [4][7]

Intensive care and the prolonged course

The intensive care course is dominated by the management of ventilatory failure and autonomic instability. He is likely to need mechanical ventilation for days to weeks, and weaning is guided by the rising forced vital capacity, the recovery of bulbar function, and the absence of fatigue. Autonomic instability is managed with careful fluid and vasopressor support and treatment of arrhythmia, and the blood pressure and heart rate are monitored continuously. Pain, which is often severe and neuropathic, is managed with gabapentin or pregabalin and with opiates where needed, and undertreated pain impedes weaning and rehabilitation. Prophylactic anticoagulation, pressure-area care, and nutrition run throughout. [10]

Prognosis, counselling, and follow-up

I would tell the family that children with Guillain-Barré syndrome recover faster and more completely than adults. A substantial majority walk independently by six months, and near-complete recovery by one year is the rule in children. I would be honest that recovery is prolonged over weeks to months, that the intensive care course is demanding, and that residual fatigue and proximal weakness can persist. I would give the family a safety-net for autonomic instability and residual deficit, and I would arrange paediatric neurology follow-up, structured physiotherapy and rehabilitation, and a gradual school return. The predictors of a poorer outcome are a rapid onset to nadir, the axonal subtypes, severe weakness at nadir, and the need for mechanical ventilation, and the Erasmus scores help set the prognosis at the bedside. [10]

Marking domains

• Diagnosis and reasoning: applies the Brighton criteria, recognises the ascending areflexic weakness, and excludes the acute flaccid paralysis mimics. [2]
• Management — resuscitation: escalates to intensive care on the spirometry numbers, secures the airway, and monitors autonomic instability. [12]
• Management — definitive: starts intravenous immunoglobulin 2 g per kg over two to five days and refuses corticosteroids. [4][7]
• Communication: counsels the family honestly on the prolonged recovery, the residual deficit risk, and the rehabilitation and school plan. [10]