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]

Question 2 (10 marks)

Discuss the differential diagnosis of acute flaccid paralysis in this child, the features that distinguish each mimic, and the prognosis and follow-up plan you would discuss with the family. [1]

The differential of acute flaccid paralysis is the practical frame, and the discriminating features are the symmetry, the reflex pattern, the presence of a sensory level, and the bowel and bladder function. This boy has the symmetrical ascending areflexic weakness with no sensory level and normal sphincter tone that fits Guillain-Barré syndrome. Transverse myelitis would show a sensory level, bladder and bowel dysfunction, and weakness below a cord level, and it needs an urgent spinal MRI and steroids. Acute flaccid myelitis is focal, asymmetric, and polio-like with anterior horn cell T2 change on MRI. Spinal cord compression from tumour, abscess, or epidural haematoma produces back pain and a sensorimotor level and is a surgical emergency. Tick paralysis is ascending and areflexic but resolves on tick removal, and botulism descends with cranial nerve palsies and dilated pupils. [1]

Because he is under fifteen years, this presentation is a notifiable public-health event that triggers stool testing for poliovirus and the exclusion of acute flaccid myelitis. I would notify the public-health unit and arrange the stool virology, and I would document the absence of cord features to justify treating without an MRI if the picture is typical. [2]

I would tell the family that children with Guillain-Barré syndrome recover faster and more completely than adults, with a substantial majority walking independently by six months and near-complete recovery by one year. I would be honest that recovery is prolonged over weeks to months, that the intensive care course is dominated by weaning ventilation and managing autonomic instability and pain, 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. [10]