Acute Flaccid Paralysis

Definition And Clinical Syndrome

Acute flaccid paralysis (AFP) is a clinical syndrome characterized by the rapid onset of weakness, progressing to maximum severity within several days to weeks.
The term ‘flaccid’ refers to the absence of spasticity or other upper motor neuron signs.
Under the Global Polio Eradication Initiative, AFP is defined as any case of flaccid weakness in children less than 15 years old, or any paralytic illness at any age when polio is suspected.

WHO Case Definition

Any child under 15 years of age with acute onset of focal weakness or paralysis characterized as flaccid (reduced muscle tone), including those in whom a clinician suspects poliomyelitis.
Any person of any age in whom poliomyelitis is suspected by a clinician.

Etiology And Anatomical Localization

Disorders presenting as AFP can localize to various points along the neuroaxis, from the anterior horn cell to the muscle.

Common Causes Of Acute Flaccid Paralysis

Anatomical Level	Examples Of Disorders
Muscle Disorders	Inflammatory myopathy, periodic paralysis, hypokalemia, severe systemic infections.
Neuromuscular Junction	Myasthenia gravis, botulism, Eaton-Lambert syndrome.
Peripheral Neuropathies	Guillain-Barré syndrome (GBS), traumatic neuritis, post-diphtheritic neuropathy, porphyria, vasculitis, Bell’s palsy.
Anterior Horn Cell	Poliomyelitis, non-polio enteroviruses.
Spinal Cord Disease	Transverse myelitis, spinal cord compression, spinal trauma.

Differential Diagnosis Of Acute Flaccid Paralysis

Differentiating the major causes of AFP is critical for management and surveillance.

Distinguishing Clinical And Laboratory Features

Feature	Poliomyelitis	Guillain-Barré Syndrome	Transverse Myelitis	Traumatic Neuritis
Progression	24-48 hours onset to full paralysis	Hours to 10 days	Hours to 4 days	Hours to 4 days
Fever At Onset	High, always present at onset; gone the following day	Not common	Rarely present	Commonly present before, during and after paralysis
Symmetry	Acute, asymmetrical, proximal	Acute, symmetrical, distal	Acute, lower limbs, symmetrical	Acute, asymmetric limb
Sensation	Severe myalgia and backache, no sensory changes	Cramps, tingling, hypoanaesthesia of palms/soles	Anaesthesia of lower limbs with sensory level	Pain in gluteal region
Deep Tendon Reflexes	Decreased or absent	Absent	Absent early; hyper-reflexia late	Decreased or absent
Bowel/Bladder	Absent	Transient, late; due to autonomic dysfunction	Present, early	Absent
Cerebrospinal Fluid	Lymphocytic pleocytosis; normal or high protein	Albuminocytologic dissociation	Variable	Normal

Algorithmic Approach


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    classDef action fill:#e8f5e9,stroke:#2e7d32,color:#2e7d32,stroke-width:2px;
    classDef polio fill:#fff3e0,stroke:#e65100,color:#e65100,stroke-width:2px;
    classDef gbs fill:#f3e5f5,stroke:#6a1b9a,color:#6a1b9a,stroke-width:2px;
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    Start[Acute Flaccid Paralysis Presentation] --> Notify[Mandatory Action: Notify Surveillance Medical Officer]:::action
    Notify --> Stool[Surveillance: Collect 2 Stool Specimens 24-48hrs apart]:::action
    Stool --> Clinical[Assess Clinical & Progression Features]

    Clinical -->|Asymmetrical, proximal weakness + Fever at onset + No sensory loss| Polio[Suspect Poliomyelitis]:::polio
    Clinical -->|Symmetrical, distal ascending weakness + No fever + Autonomic dysfunction| GBS[Suspect Guillain-Barre Syndrome]:::gbs
    Clinical -->|Symmetrical lower limb weakness + Sensory level + Early bowel/bladder issues| TM[Suspect Transverse Myelitis]:::tm
    Clinical -->|Asymmetrical limb weakness + Recent IM injection + Gluteal pain| TN[Suspect Traumatic Neuritis]:::tn

    Polio --> PolioTx[Management: Absolute bed rest, avoid IM injections]:::polio
    GBS --> GBSTx[Investigations & Mgmt: CSF analysis, NCS/EMG, IVIG or Plasmapheresis]:::gbs
    TM --> TMTx[Investigations & Mgmt: Spine MRI, High-dose Methylprednisolone]:::tm
    TN --> TNTx[Management: Pain relief, physiotherapy, conservative support]:::tn

Key Pathologies Causing Acute Flaccid Paralysis

Poliomyelitis

Clinical Presentation: Sudden onset of asymmetrical paralysis with muscle pain, predominantly involving proximal muscle groups. Febrile illness occurs just prior to paralysis.
Examination: No sensory loss; hypotonia and areflexia in the involved groups.
Management: Absolute bed rest and supportive care during the acute phase; intramuscular injections must be avoided. Later rehabilitation utilizes calipers and braces to promote ambulation.
Prevention: Full immunisation required 3-4 weeks even after a confirmed attack.

Guillain-Barré Syndrome (GBS)

Pathophysiology: Acquired post-infectious demyelinating or axonal disease of the peripheral nervous system. Campylobacter jejuni is an important preceding infection.
Subtypes: Acute Inflammatory Demyelinating Polyneuropathy (AIDP), Acute Motor Axonal Polyneuropathy (AMAN), Acute Motor and Sensory Axonal Neuropathy (AMSAN), and Miller-Fisher syndrome.
Clinical Presentation: Ascending, bilaterally symmetrical flaccid weakness, often accompanied by bilateral facial nerve weakness and autonomic dysfunction. Pain and muscle tenderness are common at onset.
Investigations: Cerebrospinal fluid demonstrates albuminocytologic dissociation (elevated protein with normal cell count). Electrophysiological studies (NCS/EMG) confirm demyelinating or axonal nerve conduction slowing.
Management: Intravenous Immunoglobulin (IVIG, 2 g/kg over 5 days) or plasmapheresis. Close observation for respiratory muscle involvement requiring ventilatory support. Corticosteroids offer no benefit and may be detrimental.

Transverse Myelitis

Clinical Presentation: Abrupt onset of symmetrical paraparesis, sensory disturbances with a distinct sensory level, and marked bladder and bowel involvement.
Evolution: Flaccidity may transition to spasticity, and hyporeflexia may be replaced by hyperreflexia after several weeks.
Investigations: MRI of the spine confirms diagnosis, typically showing cord enlargement and increased signal on T2-weighted sequences with gadolinium enhancement.
Management: High-dose methylprednisolone (1 g/1.73 m² or 30 mg/kg) started within 5-16 days of onset, given daily for 5 days.

Traumatic Neuritis

Clinical Presentation: History of intramuscular injection 1 to 5 days prior to the onset of weakness. Presents with local pain and tenderness, followed by asymmetric weakness in the injected limb.
Examination: Knee reflex may be preserved while the ankle reflex is decreased or absent. Foot drop commonly develops.
Management: Pain relief, physiotherapy, and conservative support. Usually recovers within 3-9 months.

Acute Flaccid Paralysis Surveillance Strategy

AFP surveillance is the chief strategy to screen for circulating wild poliovirus.
Notification: All patients with AFP within the last 6 months must be reported to the Surveillance Medical Officer. Cases are investigated within 48 hours of notification.

Stool Specimen Collection Protocol

Quantity: Two stool specimens must be collected. Each specimen should be approximately 8 grams.
Timing: Specimens must be collected 24-48 hours apart, ideally within 14 days of paralysis onset, though collections up to 60 days are accepted.
Transport: Specimens must be transported under strictly maintained cold chain conditions.
Laboratory Isolation: Human rhabdomyosarcoma (RD) cell lines favour enterovirus growth, whilst L20B cell lines exclusively favour polioviruses. Isolates undergo intratypic differentiation and genetic sequencing.

Virologic Classification And Quality Indicators

Classification: A case is confirmed as polio only if wild poliovirus is isolated from the stool specimen. Cases without wild poliovirus isolation but with inadequate specimens and residual weakness at 60 days undergo expert review for classification as “polio compatible” or “discarded”.
Surveillance Sensitivity: The non-polio AFP rate must be equal to or greater than 1 case per 100,000 children under 15 years per year. Additionally, an adequate surveillance program requires that at least 80% of AFP cases have two stool samples taken within two weeks of paralysis onset.

Role Of Electrophysiological Studies

Nerve Conduction Studies (NCS) and Electromyography (EMG) play a pivotal role in distinguishing true motor unit diseases from central or structural etiologies.
They differentiate anterior horn cell diseases, such as non-polio enteroviral infections (showing neuropathic denervation patterns), from neuropathies like Guillain-Barré syndrome (showing demyelinating or axonal disruption patterns).

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