Approach to a Child With Acute Flaccid Paralysis

Indian J Pediatr (October 2012) 79(10):1351 – 1357 1357 DOI 10.1007/s12098-012-0831-8

SYMPOSIUM ON PGIMER PROTOCOLS IN NEUROLOGICAL EMERGENCIES

Approach to a Child with Acute Flaccid Paralysis Sunit C. Singhi Naveen Sankhyan Ravi Shah Pratibha Singhi &

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Received: 26 January 2012 /Accepted: 8 June 2012 /Published online: 12 July 2012 # Dr. K C Chaudhuri Foundation 2012

Abstract Acute flaccid paralysis (AFP) is a clinical syndrome chara ch aracte cteriz rized ed by rap rapid id on onse sett wea weakn knes ess, s, tha thatt man many y tim times es in inclu clude dess respiratory and bulbar weakness. AFP is a broad clinical entity with an array of diagnostic possibilities. An accurate and early diagn dia gnos osis is of the ca caus usee ha hass imp import ortan antt be beari aring ng on the ma mana nagem gemen ent t and prognosis. The immediate priorities in a child who presents with acute progressive weakness are; to detect and manage respirator resp iratoryy muscle weakne weakness ss,, to detect and manage bulbar weakness,, evaluate for cardiovascular instability, weakness instability, dete detect ct and manage man age dys dyselec electro trolyte lytemia mia or toxe toxemia, mia, and to dete detect ct and man manage age a spinal compression (traumatic, intraspinal collections). Urgent imaging of the spine is needed in settings where a spinal cord involvement is suspecte suspected. d. Compressive or traumatic spinal lesions lesi ons may nee need d earl early y neu neurosu rosurgi rgical cal inte interve rventio ntion. n. Ante Anterior rior horn cell injury is usually due to direct viral infection. More distal pathologie patho logiess are gene generally rally immun immunee mediat mediated ed and respo respond nd to immunomodul immuno modulation. ation. Irrespective Irrespective of the cause, generalized generalized weakness weakn ess frequ frequently ently affects respir respiratory atory and bulb bulbar ar funct function. ion. Such children need careful monitoring and respiratory support. Keywords Polio . Acute weakn weakness ess . Paraparesis . Transverse Tran sverse myelitis . Guillain Barre syndrome syndrome

S. C. Singhi (*) : N. Sankhyan : R. Shah : P. Singhi Department of Pediatrics, Advanced Pediatrics Centre, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh 160012, India e-mail: [email protected]

Introduction

Acute fla Acute flacc ccid id pa paral ralys ysis is (AF (AFP) P) is a cli clinic nical al sy synd ndro rome me charac cha racter terize ized d by rap rapid id ons onset et wea weakn kness ess,, tha thatt fre freque quentl ntly y includes respiratory and bulbar weakness. The weakness usually usu ally pro progre gresse ssess to max maximu imum m wit within hin day dayss to wee weeks. ks. The term “flaccid” indicates the absence of spasticity or other oth er sig signs ns of dis disord ordere ered d cen centra trall ner nervou vouss sys system tem mot motor or tracts such as hype hyperreflex rreflexia, ia, clonus or exten extensor sor plantars [1]. AFP is broad clinical entity with an array of diagnostic nos tic pos possib sibili ilities ties.. An acc accura urate te and ear early ly dia diagno gnosis sis of the cause has important bearing on the management and prognosis. prognosi s. If not managed appropri appropriately, ately, paralys paralysis is can progresss to respir progres respiratory atory failur e and death. Another issue of pub public lic hea health lth imp import ortanc ancee is the imm immedi ediate ate rep report orting ing of all cases of AFP to the polio surveilla surveillance nce team(Box team(Box 1). Any cas casee mee meetin ting g the AFP def defini inition tion undergoe undergoess a thorou tho rough gh inv invest estiga igatio tion n to det determ ermine ine if the par paraly alysis sis is caus ca used ed by po poli lio. o. Ea Each ch ca case se of AF AFP P is to be re repo port rted ed and an d 2 st stoo ooll sa samp mple less (≥24 h ap apar art, t, ea each ch 8 – 10 1 0 g) ar aree colle co llecte cted d wit within hin 14 d of pa paral ralys ysis is on onse sett an and d sen sentt to WHO accre accredited dited labor laboratory atory..

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Indian J Pediatr (October 2012) 79(10):1351 – 1357

Box 1 Acute flaccid paralysis (Epidemiological definition-WHO 2005)

This protocol focuses on the clinical evaluation of a child presenting with AFP and provides a practical clinical approach to diagnosis in the Emergency department. For a detailed discussion on AFP the reader is referred to other reviews on the subject [1]. The objectives of this article are: to provide a practical approach to diagnosis in an individual patient; to provide an approach to rational use of diagnostic tests and discuss the common causes of AFP in children.

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Diagnostic Approach

Initial Assessment and Stabilization Every child with AFP is a medical emergency requiring systematic evaluation and management. Initial assessment of any such acutely ill child should concentrate on rapid cardiopulmonary assessment and resuscitation. Following are the key areas on initial assessment; &

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Detect and manage respiratory muscle weakness: Any child with acute weakness should be evaluated for res piratory muscle weakness. Younger children with respiratory muscle weakness may present with non-specific irritability, sweating, poor feeding and shallow or paradoxical respiratory efforts. Older children may complain of respiratory difficulty, may have excessive sweating, agitation, air hunger, reduced single breath count/chest expansion or shallow/paradoxical respiratory efforts. Careful serial examinations may be critical in such children to pick up the weakness early. Early elective intu bation and respiratory support are critical to save these affected children. Detect and manage bulbar weakness: Symptoms of voice change, poor cry, pooling of secretions, gurgling sounds in throat, poor ability to swallow and choking on feeds may be markers of bulbar dysfunction. Care should be taken to avoid oral feeding, providing regular suction and ensuring entral nutrition via nasogastric feeding.

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Evaluate for cardiovascular instability: Conditions leading to AFP (Spine trauma, myelitis, Guillain Barre syndrome) can also result in cardiac rhythm abnormalities and cardiovascular insufficiency. These issues will require a priority management. Hence, attaching a quadriparetic child to an ECG/cardiac monitor is an early step in the management. Rule out dyselectrolytemia or toxemia: Hypokalemia and snake envenomation are important causes of flaccid paralysis. These causes should be excluded in all children with AFP by history and examination, early in management course. A rapid assessment of electrolytes and ECG should be sought in all such children. To rule out a spinal compression (traumatic, intraspinal collections). : At the outset, patients with possible spinal injury due to trauma or other lesions requiring urgent neurosurgical intervention should be identified on history and examination. Immediate spinal stabilization and administration of corticosteroids in those with trauma would be a priority, while neurosurgical relief of spinal compression may be warranted to prevent long term disabil ity.

History The first step is to determine if an unwell child actually has muscle weakness. Many children with weakness present with nonspecific symptoms of irritability, lethargy and clumsy walk or refusal to walk. Children with abnormal gait, limp or refusing to walk may present initially to ortho pedic or trauma clinics. Pseudoparalysis due to limb pain may result from trauma, arthritis/arthralgia, myostis, joint or periosteal bleeds or joint or periartic ular infections or inflammations. It is useful to remember the possible causes of AFP in children using a neuro-anatomical approach (Table 1). Information is derived from the history and focused neurological examination looking at pattern of tone, tendon reflexes, sensory examination, signs and symptoms of bladder and/or bowel involvement. (Table 2).


Investigations

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Table 2 Selected clues in history and examination while evaluating a child with acute flaccid paralysis

The choice of the initial investigations would depend on the information gained from history and examination. Moreover, the urgency to arrive at the diagnosis would also dictate the sequence and choice of investigations. A step wise and judicious use of investigations would help reach the diagnosis with the minimum use of resources (Fig. 1). 1. MRI Spine: It is indicated when there is a suspicion of spinal cord compression or transverse myelitis. More specifically, any child with history of neck or back trauma, rapid onset flaccid profound quadreparesis, early or persistent bladder or bowel involvement, sensory loss or sensory level on examination, spinal tenderness, neurocutaneous markers, or appearance of UMN signs on examination (e.g., up going plantars) should get an MRI of the spine. 2. CSF examination: This is helpful to narrow the diagnostic possibilities. A raised CSF cell count would be seen in patients with transverse myelitis, infective myelitis viz. polio or enteroviral myelitis, varicellas or herpes myelitis, rabies, etc. A raised CSF protein with normal cell count (albuminocytological dissociation) suggests Guillain Barre syndrome, post diphtheritic

Table 1 A neuroanatomical differential diagnosis of acute flaccid paralysis in children

Points in history and/or examination

Remarks

Fever at onset

Polio or enteroviral myelitis, Transverse myelitis, myositis, epidural abscess, and Koch spine (prolonged history)

Trauma: head/neck

Trivial trauma may lead to spinal compression in patients with cervical vertebral instability (Patients with Downs syndrome, congenital cervicovertebral anomalies or juvenile idiopathic arthritis)

Exposure

Toxins: lead, arsenic Snake envenomation Dog bite: Rabies

Preceding infectious prodrome/vaccination

Guillain Barre syndrome or transverse myelitis Sore throat, neck swelling, diphtheretic polyneuropathy (non/partly immunized)

Precipitating factors

Diarrhea: Hypokalemia, enteroviral myelitis Exertion or post parandial: Hypokalemic periodic paralysis Intramuscular injection: Polio, traumatic sciatic neuritis

Sensory loss/level

Compressive myelopathy, transverse myelitis

Early bowel/bladder involvement

Compressive myelopathy, transverse myelitis

Constipation in <1 y

Botulism (H/o honey exposure)

Site

Pathophysiology

Disease

Prominent autonomic signs/symptoms

Guillain Barre syndrome, Rabies, acute myelopathy

Spinal cord

Compressive

Traumatic spinal injury, epidural abscess, hematoma, discitis

Ascending weakness

Guillain Barre syndrome, Rabies, Varicella zoster virus, ascending myelitis

Inflammatory

Transverse myelitis

Descending weakness

Diphtheria, Botulism

Viral

Poliomyelitis, vaccine associated poliomyelitis, Enteroviral myelitis, Japanese encephalitis

Prominent and early ptosis Facial weakness

Myasthenia Gravis, Botulism

Fluctuating symptoms, fatigability Muscle tenderness

Myasthenia Gravis

Muscle stretch reflexes

Absent: Guillain Barre syndrome, Polio, Diphtheria, spinal shock, at level of spinal cord damage

Anterior horn cell

Vascular Roots/nerves

Anterior spinal artery infarction

Immune mediated Guillain Barre syndrome, Toxin

Post diphth eritic, porphyria, arsenic

Viral

Rabies

Trauma

Injection related sciatic neuritis

Neuromuscular Immune mediated Myasthenia Gravis junction Drugs, toxins Organophosphates, snake venom, drugs (aminoglycosides), Botulism Infection

Viral myositis

Inflammation

Inflammatory myopathy (polymyositis)

Channelopathy

Hypokalemic periodic paralysis

Dyselectrolytemia Hypokalemia

Myositis, inflammatory myopathy, (myalgias may be severe in Guillain Barre syndrome)

Preserved : Myasthenia Gravis, periodic paralysis, Botulism Exaggerated: Below level of spinal lesion, Upper motor neuron lesion

Dyselectrolytemia Hypermagnesemia Muscle

Guillain Barre syndrome, Myasthenia Gravis, Botulism

Spinal tenderness, painful spine movement Neck stiffness

Spinal trauma, epidural abscess or other extradural compression Polio, enteroviral myelitis, Guillain Barre syndrome, transverse myelitis

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Fig. 1 Approach to child with acute paraplegia or paraparesis

Acute paraparesis/plegia

Features of spinal cord compression* / Sensory level on examination

Yes

No

CEMRI spine as early as possible

DTRs /+

Compressive myelopathy

Noncompressive myelopathy

Ocular/bulbar +

Symmetric?

involvement? +

Neurosurgery

DTR Deep tendon reflexes; CPK Creatine phosphokinase; TM Transverse myelitis; GBS Gull a i n B a r re S y n d ro m e , NC V Nerve conduction velocity; CSF Cerebrospinal fluid. *Bony tenderness/deformity, root pains, girdle sensation /early bladder or bowel involvement #other possibilities according to clinical features as described in text

consult+steroids

AcuteTM:Treat with high dosesteroidsand consult

polyneur opathy or rarely may be seen in transverse myelitis. The CSF can be normal early in the course of these illnesses. 3. Nerve Conduction studies and Electro Myography (EMG): These studies confirm the involvement of nerves and help in diagnosis of anterior horn cell diseases. These are particularly helpful to confirm Guillain Barre syndrome. The repetitive nerve stimulation test helps to diagnose myasthenia gravis and botulism. Rarely, these may aid the diagnosis of an inflammatory myopathy. 4. Creatine Kinase: Raised levels of muscle enzyme creatine kinase reflects acute muscle fiber injury and may point towards a muscle disease. In the setting of AFP this may be seen in children with viral myositis or inflammatory myopathy.

Differential Diagnosis of AFP (Table 3)

Some of the commonly encountered causes of AFP are discussed below; Guillain Barre Syndrome (GBS) With the control of polio, GBS is the most common cause of AFP in children. Worldwide its incidence is 0.6 – 4 cases per 100,000 per year [2]. It most commonly occurs after an

Myasthenia, Botulism

GBS#

CPK,K+, Urine myoglobin

Polio, GBS, Traumatic neuritis. Get NCV Viral myositis, periodic paralysis, Rhabdomyolysis

IVIG,Neuro consult,NCV, CSF

infection triggered immune mediated attack on the nerve axons or myelin. Antecedant respiratory or gastrointestinal illnesses are commonly found in the history [3]. The most common underlying subtype of the syndrome is the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) but the other common subtype of acute motor axonal neuropathy (AMAN) may be equally common in Indian children [4]. In the typical cases, the first symptoms are usually pain, paraesthesia, or weakness in the limbs which spreads proximally. Weakness may progress rapidly, and approximately 50 % of the children will reach nadir by 2 wk, 80 % by 3 wk, and the rest by 4 wk. Risk factors for children requiring ventilation are cranial nerve involvement, increased CSF protein during first week of illness and short period between antecedent illness and the onset of symptoms [5]. Investigations required for confirming the diagnosis are; nerve conduction studies and lumbar puncture (to document CSF albumin-cytological dissociation). A raised CSF protein concentration is present in about 80 % of patients, but CSF protein content is more likely to be normal during the first days of the illness [3]. When a child presents in the acute phase, the differentiation from polio or enetroviral myelitis can be done based on CSF. Viral myeltis would show CSF pleocytosis, which would be conspicuously absent in GBS. CSF should be analyzed before treatment with intravenous immunoglobulin (IVIG) as IVIG can cause aseptic meningitis. Management of a child with GBS would involve a meticulous observation for respiratory, bulbar muscle weakness. Early elective intubation and ventilatory support are important in the acute phase. During hospitalization, monitoring for


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Table 3 Characteristics to aid differential diagnosis of acute flaccid paralysis

Feature

Transverse myelitis

Development of paralysis Fever at onset of weakness Paralysis Progression of paralysis Muscle tone Deep-tendon reflexes Sensation

Cranial nerve involvement Respiratory insufficiency Autonomic signs and symptoms

Guillain-Barre syndrome

Traumatic neuritis (following injection)

From hours to four days 24 to 48 h from onset to full paralysis May be present High, always present at onset of flaccid paralysis

From hours to 4 wk

From hours to four days

Uncommon

Present, if underlying infection being treated with IM injections

Symmetric

Asymmetric,

Symmetric, mostly ascending

Affects only one limb

Descending

Ascending

Reduced

Reduced

Reduced

Decreased or absent

Absent

Decreased or absent

Severe myalgia, backache, no sensory changes

Cramps, tingling, hypoanesthesia of palms and soles

Pain in gluteus

Only when bulbar involvement is present Only when bulbar involvement is present Rare

Often present, affecting nerves VII, IX, X, XI, XII Occurs in severe cases

Absent

•

Reduced during acute phase Absent in lower limbs(early); hyperreflexia(late) Anesthesia of lower limbs with sensory level Absent Sometimes Present

Cerebrospinal fluid

Normal or Pleocytosis

Bladder dysfunction

Present- early and persistent Normal

Nerve conduction velocity: third wk

Diagnostic test

Poliomyelitis

MRI spine –

Mild elevation of lymphocytes 10 to 200/mL Rare

Absent

Frequent in severe cases (blood pressure Hypothermia in alterations, sweating, blushing, and affected limb body temperature fluctuations) Albumin-cytologic dissociation (usually Normal <10 cells/ml, never >50cells/ml) Occasionally (Transient, at the peak of weakness, 1 3 d (30 %)) Abnormal: slowed conduction, decreased motor amplitudes

Never

Nerve conduction studies

Nerve conduction studies, Electromyography

–

Abnormal: anterior horn cell disease (normal during first 2 wk) Stool viral detection

Abnormal: s/o motor-sensory axonal damage

Adapted and modified from Global Program for Vaccines and Immunization: Field Guide for Supplementary Activities Aimed at Achieving Polio Eradication. Geneva, World Health Organization, 1996

autonomic instability and prevention of nosocomial complications are essential to optimize outcomes. IVIG is the treatment of choice in the authors’ setting for GBS, given the availability, ease of administration and the safety compared with plasmapheresis. It is given in the dose of 2 g/kg spread over 2 – 5 d. Anterior Horn Cell Viral Myelitis Poliomyelitis Both the wild polio virus and the vaccine associated polio virus cause anterior horn cell affliction to result in flaccid paralysis. Children under 5 y are the most frequently affected. However, older individuals and adults can also develop

poliomyelitis. The initial symptoms of polio are non-specific and include fever, headache, vomiting, constipation, neck stiffness and pain in limbs. The paralysis follows or accom panies these symptoms. The maximal weakness evolves quickly over 1 – 2 d. A history of intramuscular injections precedes paralytic poliomyelitis in about 50 – 60 % of patients, patients may present initially with fever and paralysis (provocation paralysis). Clinical characteristics of poliomyelitis include; 1. Fever at onset 2. Rapid progression of paralysis within 24 – 48 h 3. Asymmetric, proximal more than distal limb paralysis 4. Preservation of sensory function often with severe myalgias 5. Residual paralysis at 60 d [6]. Most of the children with paralytic polio die from complications of bulbar paralysis and respiratory failure. Management is mainly focused on meticulous supportive care.

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Non Polio Enteroviral Myelitis

Table 4 Summary of approach to diagnosis in a child with acute flaccid paralysis

Non polio enteroviruses can cause a polio like paralytic disease. Among all known nonpolio enteroviruses, enterovirus-71 has been most strongly implicated in out breaks of central nervous system disease and AFP. The clinical syndrome frequently is associated with aseptic meningitis, hand, foot and mouth disease and hemorrhagic con junctivitis [7]. Weakness associated with enterovirus disease can be severe and permanent.

1. ABCs ●

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Check and support: BP and Heart Rate

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Immobilize neck if history of neck/head trauma

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Send electrolytes and get an ECG- to look for hypokalemia

2. Examination and classification into pattern for example, ●

Flaccid Paraparesis with sensory level (early bladder dysfunction)Transverse myelitis, compressive myelopathy

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Flaccid afebrile symmetric para/quadriparesis (+/ − bulbar and respiratory involvement) with areflexia and minimal sensory loss (but often sensory symptoms) : Acute neuropathy or polyradiculopathy (esp., Guillain Barre Syndrome)

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Flaccid, febrile, pure motor, asymmetric, paralysis (no bladder involvement) often with meningismus: Enteroviral, polio, or vaccine associated poliomyelitis

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Flaccid motor-sensory lower limb monoparesis after IM injection: Injection neuritis

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Ophthalmoplegia, ptosis, bulbar weaknes with motor weakness: Miller-Fischer variant of Guillain Barre Syndrome, Botulism, Myasthenia Gravis

Other Viruses Causing AFP Rabies The common presentation of human rabies is with fever, behavioral and autonomic instability and hydro/aero phobia. However, a minority of the patients can present primarily with paralytic disease. This type of presentation follows a prodrome of paraesthesias in the bitten area, ascending paralysis or paralysis progressing from the bitten limb. Sphincter disturbances and autonomic instability is common. Disease progression is slower in paralytic rabies [8]. The disease can be easily missed if a history of animal bite is not actively sought. Frequently the bite may not be recent and the parents may not give the history, unless specifically asked for. Herpes group of viruses can lead to AFP by triggering GBS or transverse myelitis, causing polyradiculoneuropathies in immunocompromized hosts [9]. Japanese encephalitis virus can also preferentially affect the anterior horn cell and cause paralysis associated with encephalitis [10].

Ensure protection of airway and adequate ventilation (especially if there is respiratory muscle weakness, shallow respiration, dysphagia, weak gag)

Proximal muscle weakness, muscle tenderness without sensory symptoms or signs and with preserved reflexes: Viral myositis, Inflammatory myopathy (e.g., dermatomyositis)

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3. Investigations (according to the suspected site of lesion and cause of paralysis) ●

Neuroimaging (spinal cord) MRI indicated in all cases of myelopathy, suspected transverse myelitis

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X- ray spine: suspected atlantoaxial dislocation, vertebral tuberculosis

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Transverse Myelitis It is an acute demyelinating disorder of the spinal cord. It may occur alone or in combination with demyelination in other portions of the nervous system. It is believed commonly that previous infection or immunization triggers transverse myelitis, but no evidence supports such a notion [11]. The common presentation includes an acute phase of spinal shock with flaccid paraparesis or quadreparesis, urinary retention or incontinence, absent reflexes and mute plantars, sensory loss/level is frequently present. After a few weeks, the signs of UMN dysfunction appear, in the form of spasticity, and hypereflexia. This disorder should be suspected in any child with rapid onset flaccid profound quadreparesis, early or persistent bladder or bowel involvement, sensory loss or sensory level on examination, with suggestion of UMN signs on examination (e.g., up going plantars). In such a situation an urgent spinal MRI is needed to establish the diagnosis. Other causes of acute myelopathy like trauma, paraspinal/epidural spinal abscess, hematoma or anterior spinal artery syndrome need exclusion in this setting. The management of transverse

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Electrophysiologic testing (NCV & electromyography): Guillain Barre syndrome

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Lumbar puncture (CSF): Guillain Barre syndrome, suspicion of viral myelitis

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Biochemistry: Creatine Kinase, Potassium, Magnesium, Phosphate

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ECG : Hypokalemia

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Urine for porpho-bilinogens in porphyria, toxins: arsenic

4. Management (depends on the underlying etiology identified) ●

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All children: meticulous supportive care, anticipate and identify respiratory, bulbar weakness (except in injection neuritis), shock due to reduced vascular tone (spinal cord disease), Autonomic instability, complications of immobilization and prevention of nosocomial infections. Specific therapy:

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Guillain Barre syndrome: IVIG, 2 g/kg over 2 5 d –

Transverse myelitis: IV methy-prednisolone 10 30 mg/kg, daily (max-1 g) for 3 5 d

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○ Compressive myelopathy: spinal immobilization, surgical intervention, steroids (acute traumatic myelopathy) ○

Dermatomyositis, Myasthenia Gravis: Immunomodulation

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Hypokalemia: Intravenous potassium correction


myelitis consists of immunosuppression and supportive care. Attention is needed to maintain airway, breathing and circulation, bladder catheterization and exclusion of compressive myelopathy by imaging. High dose pulse corticosteroids are the recommended form therapy [11]. Methylprednisolone is given in a dose of 10 – 3 0 mg/kg/d (max:1 g/d) for 5 d followed by oral prednisolone 1 – 2 mg/kg/d for 2 wk and then tapered over subsequent 2 – 4 wk.

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(snake bite). Evaluation of spine by imaging may be needed urgently in patients with suggestive clinical features. Once these causes are excluded, most distal pathologies are generally immune mediated and respond to immunomodulation. Irrespective of the cause, generalized weakness frequently affects respiratory and bulbar function. Such children need to be carefully monitored and treated.

Traumatic Neuritis (Following Injection) Conflict of Interest

Traumatic neuritis is suspected in cases in which there is one limb involvement and definite history of injection in that limb (usually less than 24 h) before the onset of paralysis. It is associated with pain and hypothermia of affected limbs. It is sometimes difficult to distinguish it from polio. However, sensory deficits and lack of CSF pleocytosis favor the diagnosis of traumatic neuritis. It is probable that some cases of polio are misdiagnosed as traumatic neuritis. Residual sensory deficits strongly favor the diagnosis of injection neuritis. Management is entirely supportive. Hypokalemic Paralysis This is an important differential in any child particularly in a younger child with AFP. An early recognition can prevent potentially fatal cardiac complications. In the developing countries, it most commonly results from diarrheal diseases. However, rarer familial chanellopathies, underlying disorders, such as renal tubular acidosis, primary/secondary hyperaldosteronism also need to be considered. Correction of potassium levels rapidly reverses the paralysis in these children.

Conclusions

AFP is a broad clinical entity with an array of diagnostic possibilities. Every case of AFP is a medical emergency. A systematic anatomic/pathophysiological approach to diagnosis helps to narrow down the diagnostic possibilities in a given child (Table 4). Accurate and early diagnosis of the cause has important bearing on the management and prognosis. The immediate priorities are to detect and manage respiratory, bulbar muscle weakness, rapidly exclude causes which are reversible like dyselectrolytemia or toxemia

None.

Role of Funding Source

None.

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Approach to a Child With Acute Flaccid Paralysis

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