Guillain-Barré syndrome and acute flaccid paralysis

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Target exams

Red flags

• A previously well child with progressive ascending flaccid weakness and absent reflexes has Guillain-Barre syndrome until proven otherwise, not a viral myalgia
• Measure bedside forced vital capacity every two to six hours; a value under twenty millilitres per kilogram or a fall of greater than thirty percent mandates intensive care
• Bulbar weakness with a weak cough and pooled secretions predicts aspiration and ventilatory failure; secure the airway early
• Do not give corticosteroids for Guillain-Barre syndrome; the systematic review shows no benefit and possible harm
• A sensory level, bladder or bowel dysfunction, or asymmetric weakness argues for transverse myelitis or acute flaccid myelitis, not Guillain-Barre syndrome; get an urgent spinal MRI
• Acute flaccid paralysis in a child under fifteen years is a notifiable public-health event that triggers stool testing for poliovirus

Life stages

Care settings

Clinical exam formats

Board mappings

• Recognises Guillain-Barre syndrome as the commonest cause of acute flaccid paralysis in a previously well child and states that weakness ascends symmetrically over days with areflexia
• States that intravenous immunoglobulin 2 g per kg over two to five days is first-line and that corticosteroids are not recommended
• Identifies the respiratory red flags of falling forced vital capacity and bulbar weakness and the need for intensive care monitoring
• Applies the Brighton diagnostic criteria and the Asbury Cornblath criteria and distinguishes AIDP from AMAN, AMSAN, and the Miller Fisher syndrome
• Justifies the choice of intravenous immunoglobulin over plasma exchange using the van der Meche trial and the Cochrane evidence and explains why corticosteroids are ineffective or harmful
• Uses the Erasmus Respiratory Insufficiency Score and the modified Erasmus Outcome Score to predict ventilation and outcome and times intensive care escalation
• The Brighton diagnostic levels and the albuminocytological dissociation in the cerebrospinal fluid
• The subtypes AIDP, AMAN, AMSAN, Miller Fisher, and Bickerstaff brainstem encephalitis and their antibody associations
• The intravenous immunoglobulin dose of 2 g per kg over two to five days, the plasma exchange alternative, and the corticosteroid contraindication
• Runs the assessment, respiratory monitoring, and first-line treatment of a child with ascending paralysis and areflexia while excluding the acute flaccid paralysis mimics
• Decides on and times intensive care escalation using forced vital capacity and bulbar and autonomic monitoring, and coordinates retrieval to a tertiary centre
• Counsels the family on the cause, the prolonged recovery over months, the residual deficit risk, and the rehabilitation plan
• Level 1: Recognition that acute ascending flaccid weakness with areflexia in a previously well child is Guillain-Barre syndrome until proven otherwise
• Level 2: Application of the diagnostic criteria, the cerebrospinal fluid and neurophysiology, and the intravenous immunoglobulin dose and respiratory monitoring
• Level 3: Coordination of intensive care, the differential of acute flaccid paralysis including transverse myelitis and acute flaccid myelitis, and the rehabilitation and recovery course
• Guillain-Barre syndrome as the commonest acute flaccid paralysis in children, its post-infectious mechanism with Campylobacter jejuni molecular mimicry, and its ascending symmetrical areflexic presentation
• The Brighton diagnostic criteria, albuminocytological dissociation, and the subtypes including the Miller Fisher syndrome with its anti-GQ1b antibody
• The first-line intravenous immunoglobulin dose, the respiratory monitoring with forced vital capacity, and the lack of benefit of corticosteroids
• Structured assessment of a child with progressive ascending weakness, including bedside spirometry and bulbar and autonomic monitoring
• Recognition of intensive care triggers and the timing of intravenous immunoglobulin, and the exclusion of acute flaccid myelitis and transverse myelitis
• Communication of the diagnosis, the prolonged recovery, and the rehabilitation plan to the family
• Guillain-Barre syndrome as the commonest cause of acute flaccid paralysis in United States children and its Campylobacter jejuni antecedent
• Intravenous immunoglobulin 2 g per kg over two to five days as first-line therapy with respiratory monitoring, and the exclusion of acute flaccid myelitis
• The subtypes, the albuminocytological dissociation, and the Erasmus prognostic scores for ventilation and outcome
• Recognition of acute ascending flaccid paralysis with areflexia as Guillain-Barre syndrome and the exclusion of acute flaccid myelitis, transverse myelitis, and tick paralysis
• Stepwise management with respiratory monitoring, intravenous immunoglobulin, and intensive care escalation
• Multidisciplinary care of autonomic instability, pain, prolonged ventilation, and rehabilitation
• Canadian approach to acute flaccid paralysis surveillance and the diagnosis of Guillain-Barre syndrome using the Brighton criteria
• Intravenous immunoglobulin 2 g per kg and respiratory monitoring with forced vital capacity thresholds for intensive care
• Coordination of intensive care, rehabilitation, and long-term follow-up including residual deficit and relapse surveillance