Describe the acute Flaccid Paralysis of Guillain-Barré Syndrome.

Definition

• Guillain-Barré syndrome (GBS) is an acute, immune-mediated demyelinating polyradiculoneuropathy causing rapidly progressive ascending flaccid paralysis.
• In the post-polio era it is the commonest cause of acute flaccid paralysis (AFP) in children.

Etiology & Pathogenesis

• Typically post-infectious — 1–3 weeks after a respiratory or gastrointestinal infection (classically Campylobacter jejuni; also viral).
• Molecular mimicry — antibodies against the pathogen cross-react with peripheral nerve myelin/axons → immune-mediated nerve damage.

Clinical Features

• Ascending, symmetrical flaccid weakness — starting in the legs and progressing upward over days.
• Areflexia / hyporeflexia (a key sign).
• Respiratory muscle involvement (may need ventilation) and bulbar weakness (swallowing/speech) — the dangerous features.
• Autonomic instability — labile blood pressure, arrhythmias, sweating.
• Sensory symptoms are usually mild; sphincter function is typically preserved.

Differential Diagnosis of Acute Flaccid Paralysis

Investigations

• CSF — albuminocytological dissociation (raised protein with a normal/near-normal cell count) — characteristic (may be normal in the first week).
• Nerve conduction studies — features of demyelination (slowed conduction, conduction block).
• Exclude other causes of AFP (stool for poliovirus in surveillance; imaging for cord lesions).

Management

• Supportive care is paramount — monitor respiratory function (vital capacity) and provide ventilation if it deteriorates; protect the airway if bulbar weakness.
• Monitor autonomic function (cardiac monitoring); manage blood-pressure lability and arrhythmias.
• Immunotherapy — IV immunoglobulin (IVIG) or plasmapheresis (equally effective) to shorten the illness and improve recovery.
• Physiotherapy, DVT prophylaxis, pain management and nutritional support during recovery.

Prognosis

• Most children recover completely or with minimal deficit over weeks to months, as the peripheral nerves remyelinate.
• The main acute risks are respiratory failure and autonomic instability, which is why close monitoring in the acute phase is essential.
• GBS is a notifiable AFP for polio-surveillance purposes.

Clinical Variants

• Miller Fisher syndrome — ophthalmoplegia, ataxia and areflexia.
• Acute motor axonal neuropathy (AMAN) and other axonal variants; pharyngeal-cervical-brachial variant.

Monitoring (the Crux of Care)

• Serial vital capacity / respiratory function — the key to timing ventilation.
• Continuous cardiac monitoring for autonomic arrhythmias; blood-pressure lability.
• Bulbar function (safe swallow) to prevent aspiration.

Complications

• Respiratory failure requiring ventilation; aspiration pneumonia.
• Autonomic instability — arrhythmias, labile BP; immobility complications (DVT, pressure sores).

Factors Affecting Recovery

• Most children recover well; a rapid onset, need for ventilation, and axonal (rather than demyelinating) forms are associated with slower or less complete recovery.
• Because GBS is the main cause of AFP, every case must be reported and investigated to exclude poliomyelitis.

Supportive Care During Recovery

• Physiotherapy and graded mobilisation to prevent contractures and regain strength.
• DVT prophylaxis, pressure-area care, bladder/bowel care, and pain management (neuropathic pain is common).

WHY It Matters for Polio Surveillance

Because GBS is the leading cause of acute flaccid paralysis, every case in a child under 15 years must be notified and investigated (with stool samples for poliovirus) as part of the national polio-surveillance programme, even when GBS is the obvious clinical diagnosis.