Indian Academy of Pediatrics (IAP)
NATIONAL TREATMENT
GUIDELINES
Chairpersons
GV Basavaraja
President 2024
Vasanth Khalatkar
President Elect 2024
IAP Coordinators
Yogesh Parikh
Hon Secretary General 2024–25
Acute Flaccid Atanu Bhadra
Treasurer 2024–25
Paralysis National Coordinator
Arun Bansal
Bela Verma National Convenors
Meghana Tiwary Vinod H Ratageri
Vishnu Mohan PT
Zonal Coordinators
Sheikh Minhaj Ahmed
Mihir Sarkar
Suresh Kumar Angurana
Sasidaran Kandasamy
Mounika Reddy
37 Acute Flaccid Paralysis
INTRODUCTION
Acute flaccid paralysis (AFP) is a complex clinical syndrome with a multifactorial etiology.
Each case is an emergency, both in terms of the need for appropriate, correct treatment and AFP
surveillance.
India has been polio-free since 2014;1 however, AFP surveillance is an important tool for the early
detection and prevention of the community spread of polio.
The number of AFP (AFP from nonpolio causes) cases in 2023 in India was 7.46/100,000 cases.2
TERMINOLOGIES AND DEFINITIONS
Acute flaccid paralysis is an acute onset flaccid weakness of <14 days, reaching its maximum severity
in days to weeks.
An AFP case is defined as a child under 15 years presenting with sudden onset of floppy paralysis
or muscle weakness due to any cause, or any person of any age with paralytic illness if a clinician
suspects poliomyelitis.3 The etiopathology of AFP is given in Table 1.
Acute Flaccid Paralysis
ETIOPATHOLOGY
TABLE 1: Etiopathology of acute flaccid paralysis.
Central Anterior Neuromuscular
causes Spinal horn cell Peripheral nerve junction Muscle
Brainstem Acute transverse Poliomyelitis Guillain–Barré Syndrome Myasthenia Viral myositis
encephalitis myelitis (radiculopathy)
ADEM, NMO Acute Nonpolio Traumatic neuritis Botulism Hypokalemic
myelopathy enterovirus periodic paralysis
Stroke Cord Rabies Toxic neuropathies Snakebite McArdle disease
compression (diphtheria, tick bite, lead,
syndrome and arsenic)
Tumor Varicella Critical illness neuropathy Organophosphorus Polymyositis
Zoster poisoning
Abscess Drug-induced Critical illness
myopathy
Cerebral acute intermittent
sinus Venous porphyria
thrombus
(ADEM: acute disseminated encephalomyelitis; NMO: neuromyelitis optica)
Fig. 1: Single motor unit.4
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Acute Flaccid Paralysis
CLINICAL FEATURES
The clinical presentations are as follows:
Presenting history:
Inability to walk or stand
Weakness of upper and lower limbs, usually associated with severe limb pain
Breathing difficulty
Difficulty in swallowing
Change in voice
Facial deviation
Loss of bowel/bladder control
Based on onset:
Hyperacute: Few minutes—vascular pathology
Acute: Few hours—Guillain–Barré syndrome (GBS), polio, and acute transverse myelitis
Insidious: Few days—tick paralysis
Based on progression:
Ascending paralysis: Lower limbs-upper limbs; can be symmetrical (GBS) or asymmetrical (polio)
Descending paralysis: Bulbar muscles-upper limbs-lower limbs-post diphtheria paralysis, and
botulism
Episodic paralysis: Complete recovery between episodes-hypokalemic periodic paralysis
Recurrent paralysis: CACNA1A-related channelopathies
Clinical clues for diagnosis (Table 2)
TABLE 2: Clinical clues for diagnosis.
Clinical history and examination Diagnosis
Preceding diarrheal illness Guillain–Barré syndrome
History of bull neck, fever, and throat pain in preceding weeks Postdiphtheria polyneuropathy
Recent intramuscular injection Traumatic neuritis
Trauma to spine/neck Traumatic myelopathy
Recent dog bite/travel to hilly areas Rabies/tick-bite paralysis
History of consumption of canned goods/ingestion of contaminated honey Botulism
Predominant sensory symptoms Occupational exposures: Arsenic and lead
(paresthesia, numbness, tingling sensations, and abdominal pain)
Similar episodes in the past, history of nonspecific abdominal pain, and Acute intermittent porphyria
photosensitivity
Sudden onset weakness in the morning after carbohydrate-rich meal Hypokalemic periodic paralysis
in the night
History of prolonged ICU stay, use of corticosteroids, and use of Critical illness polyneuropathy
neuromuscular blockade drugs (e.g., vecuronium)
4 Onset of weakness immediately after heavy exercise or running Glycogen storage disorders
Acute Flaccid Paralysis
Diagnosis based on pattern of central nervous system involvement (Table 3): 5
TABLE 3: Pattern of central nervous system involvement and the diagnosis.
Pattern Diagnosis
Asymmetric and patchy motor weakness with complete sensory sparing Poliomyelitis
Symmetric motor ascending weakness with or without sensory Guillain–Barré Syndrome (GBS)
involvement
Ptosis, extraocular weakness, and diplopia with diurnal variation Myasthenia gravis (present as myasthenic crisis)
Muscle weakness with sudden ptosis, and EOM weakness Snakebite (neurotoxic) and rabies (dumb rabies)
Bulbar onset of weakness Postdiphtheria polyneuropathy or botulism
Cranial nerve involvement Tick paralysis, postdiphtheria polyneuropathy,
GBS, acute flaccid myelitis, and Lyme disease
Early bladder involvement (retention) Acute transverse myelitis and GBS (15%)
The approach to diagnosing AFP is illustrated in Flowchart 1.
Flowchart 1: Algorithm to diagnosis.
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Acute Flaccid Paralysis
INVESTIGATIONS
Acute flaccid paralysis surveillance: A country’s surveillance system needs to be sensitive enough to
detect at least one nonpolio AFP case each year for every 100,000 children aged under 15 years.
Global Polio Eradication Initiative (GPEI) aims to confirm and sequence all polioviruses
within 35 days of the onset of paralysis. The process from onset of paralysis to the arrival of
stool specimens at a World Health Organization (WHO)-accredited polio laboratory must be
completed within 14 days (Flowchart 2).
Flowchart 2: Acute flaccid paralysis surveillance.
Nerve conduction studies (Flowchart 3): Test results can be normal at onset of illness; hence, it is
best to repeat after 2–3 weeks.
Flowchart 3: Nerve conduction study results.
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Acute Flaccid Paralysis
Cerebrospinal fluid (CSF) studies: These help identify etiology and support the diagnosis, although
does not confirm it. It is done in 2nd–3rd week of illness.
Magnetic resonance imaging (MRI) brain + spine: It is a supportive investigation and can help
localize various demyelinating disorders. For example, nerve root enhancement in GBS
Blood investigations: Complete blood count, erythrocyte sedimentation rate (ESR), electrolytes,
and creatine phosphokinase (CPK).
Specific investigations: According to clinical suspicion, for example, blood-lead levels.
DIFFERENTIAL DIAGNOSIS OF
ACUTE FLACCID PARALYSIS
Differential diagnoses of acute flaccid paralysis are given in Table 4.6
TABLE 4: Differential diagnosis of acute flaccid paralysis and their characteristics.
Characteristics Poliomyelitis Guillain–Barré syndrome Traumatic neuritis Transverse myelitis
Site involved Anterior horn cell Nerve root Peripheral nerve Spinal cord
Progression of paralysis 24–48 hours Hours to days Hours to days Hours to days
Distribution of weakness Asymmetric Symmetric ascending Along distribution Symmetric lower limb
patchy of involved nerve
Deep tendon reflexes Absent Absent Decreased/absent Absent early
Hyperreflexia late
Babinski reflex Absent Absent Absent Present
Sensory involvement Myalgia + Cramps, tingling, and Pain along nerve Anesthesia of lower
No sensory hypoesthesia of palms distribution (gluteal limbs with sensory
involvement and soles region in cases of level
intramuscular (IM)
injection)
Cranial nerve +/– +/– – –
involvement
Respiratory insufficiency + In cases of In severe cases Absent Sometimes involved
bulbar and
bulbospinal
involvement
Bladder involvement Absent Transient Absent Present
(retention)
Contd…
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Acute Flaccid Paralysis
Contd…
Characteristics Poliomyelitis Guillain–Barré syndrome Traumatic neuritis Transverse myelitis
CSF examination Cell count raised; <10 leukocytes, high Normal Cell count – normal/
Protein normal/ protein, slight increase in
slightly increased Albuminocytological lymphocytes
dissociation Proteins: normal/
slightly raised
EMG (3 weeks) Abnormal Normal May be abnormal Normal
NCV (3 weeks) Normal Abnormal, Abnormal Normal
Demyelination/axonal
Sequelae Severe asymmet- Symmetrical distal limb Moderate atrophy Diplegia and atrophy
rical atrophy atrophy of affected muscle after many years
(CSF: cerebrospinal fluid; EMG: electromyography; NCV: nerve conduction velocity)
EMERGENCY CARE
The algorithmic approach to emergency care is given in Flowchart 4.
Flowchart 4: Algorithm for emergency care.7
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Acute Flaccid Paralysis
SPECIFIC TREATMENT
The specific treatment for different cases of AFP is given in Table 5.
TABLE 5: Specific treatment.
Guillain–Barré Syndrome Intravenous (IV) immunoglobulin 2 g/kg
Transverse myelitis y Methylprednisolone 30 mg/kg/day for 3–5 days;
y Plasma exchange or intravenous cyclophosphamide (800–1,200 mg/m2) administered
as a single pulse dose
Snakebite Antisnake venom and trial of atropine and neostigmine
Botulism Treatment with antitoxin
Lead poisoning EDTA chelation therapy
(EDTA: ethylenediaminetetraacetic acid)
SUPPORTIVE MANAGEMENT
The supportive management includes:
Neutral position of limbs and splinting to prevent contractures
Regular change of posture to prevent bed sores
Chest and limb physiotherapy
Urinary retention—catheterization
Pain—appropriate analgesics
Nutritional rehabilitation
MONITORING
Monitoring involves the following:
Vitals: Assessment of autonomic instability
Muscle charting: To monitor progression of weakness and power of muscles
Gag reflex: To assess bulbar involvement
Deep tendon reflexes: To assess clinical improvement
Checking for bed sores and contractures
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Acute Flaccid Paralysis
KEY LEARNING POINTS
AFP is a diagnostic dilemma, and it is important to carefully evaluate each case to establish a
diagnosis.
AFP surveillance is an essential part of the healthcare system and is the pillar of polio eradication
in India.
REFERENCES
1. The National Department of Health, South Africa, Expanded Programme on Immunisation. (2015). EPI
Diseases Surveillance Guideline, 3rd Edition (2015). [online] Available from https://www.nicd.ac.za/assets/
files/EPI%20Surveillance%20Manual_15Dec2015.pdf [Last accessed November, 2024].
2. Our World in Data. (2024). Rate of acute flaccid paralysis from non-polio causes. [online] Available from
https://ourworldindata.org/grapher/rate-of-acute-flaccid-paralysis-from-non-polio-causes?country=AFG~
PAK~MWI~MOZ~BWA~RWA~KEN~IND [Last accessed November, 2024].
3. World Health Organization. (2023). Global guidelines for acute flaccid paralysis (AFP) surveillance in the
context of poliovirus eradication. Prepublication version. [online] Available from: https://polioeradication.
org/wp-content/uploads/2023/03/Global-AFP-guidelines-pre-publiucation-version-2023.pdf
[Last accessed November, 2024].
4. Webster JG, Clark JW. Medical Instrumentation: Application and Design, 4th edition. Hoboken, NJ: John
Wiley & Sons; 2010.
5. Clinical Approach to Paediatric Neurology [Internet]. Google Books. 2021 [cited 2024 Sep 15]. Available
from: https://books.google.co.in/books/about/Clinical_Approach_to_Pediatric_Neurology.html?id=KiEuzg
EACAAJ&redir_esc=y
6. Kunju M, Subir A, Eapen M. Acute flaccid paralysis beyond polio-a case-based approach. Indian Journal
of Practical Paediatrics [Internet]. 2020;22(1):36. Available: https://www.ijpp.in/Files/2020/ver1/Acute%20
flaccid%20paralysis%20beyond%20polio%20-%20A%20case%20based%20approach.pdf
7. Acute Flaccid Paralysis in Adults [Internet]. [cited 2024 Sep 15]. Available from: https://www.jipmer.edu.in/
sites/default/files/Acute_flaccid_paralysis_Protocol-final-2.pdf
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