Indian Journal of Practical Pediatrics 2020;22(1) : 36

NEUROLOGY

ACUTE FLACCID PARALYSIS BEYOND Acute flaccid paralysis (AFP) is an acute onset flaccid
POLIO- A CASE BASED APPROACH weakness, less than 4 weeks, reaching its maximum severity
in days to weeks. Some of the causes of AFP are Guillain-
*Mohammed Kunju PA Barre syndrome (GBS), poliomyelitis, transverse myelitis
**Ahamed Subir H (TM), traumatic neuritis and post diphtheritic neuropathy.
***Merin Eapen Continued surveillance of AFP is required to completely
eradicate poliomyelitis. A case for surveillance of AFP is
Abstract: Acute flaccid paralysis is a complex clinical
defined as any case of AFP in children <15 year old, or
syndrome that requires immediate and careful evaluation
any paralytic illness at any age when polio is suspected.
for making a diagnoses. Each case of acute flaccid
Many reviews are available on AFP and this article outlines
paralysis is an emergency from both clinical as well as
a case based approach, to highlight the varied presentation.
public health perspective. The precise knowledge of the
etiology, underlying pathophysiology and concurrent Etiologies of AFP1
changes have profound implications in the treatment and
prognosis. With the eradication of polio, Gullian Barrie It is easier to analyse the cause based on anatomic
Syndrome has become the major acute flaccid paralysis. location
Seasonal occurrence of Gullain Barrie Syndrome with spurt
 Brain stem: GBS with cranial nerve involvement, brain
of viral fever is also seen. However, the clinical features of
stem encephalitis and stroke
polio must be taught to the younger residents since
imported or vaccine associated polio can still occur.  Spinal cord: Acute transverse myelitis, acute
Better usage of Magnetiic resonance imaging scanning will myelopathy due to spinal cord compression (abscess,
help in establishing the diagnosis. Acute management of space occupying lesion), anterior spinal artery
such patient with acute flaccid paralysis due to different syndrome.
causes in intensive care unit has become a necessity.  Anterior horn cells: Poliomyelitis, non-polio
Based on severity IVIg for Gullain Barrie Syndrome and enteroviruses.
Methyl prednisolone for transverse myelitis are now
accepted protocols. We are still in the process of  Nerve root (radiculopathy): Guillain Barre syndrome.
consolidating the eradication of polio by the endgame  Peripheral nerve: Guillain Barre syndrome, toxic
strategy from 2019-2023. neuropathies (diphtheria, tick bite paralysis, lead,
arsenic poisoning) traumatic neuritis, acute
Keywords: Acute flaccid paralysis, Guillain-Barre intermittent porphyria, critical illness neuropathy.
Syndrome, Lower motor neuron localization, Transverse
myelitis  Neuromuscular junction: Myasthenia gravis, botulism,
snake bite, organophosphorus poisoning.
 Muscle: Polymyositis, trichinosis, hypokalemia,
* Professor and Head, hypophosphatemia.
Dept of Pediatric Neurology, Clinical approach
Medical College, Trivandrum
** Assistant Professor, Usually sudden occurrence of flaccid weakness
Dept of Neurology, MES Medical College, denotes lower motor neuron (LMN) weakness. However,
Perinthalmanna, Malappuram upper motor neuron (UMN) weakness of sudden onset also
*** Senior Resident can have flaccid weakness in the initial stages due to the
Dept of Pediatric Neurology, neuronal shock state. Following a systematic clinical
Medical College, Trivandrum approach based on the distribution and progression of
email : [email protected] weakness, associated sensory involvement, fever etc. will
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Indian Journal of Practical Pediatrics 2020;22(1) : 37

help in differentiating various conditions. Gradual onset eradication of polio, new viral infections can present as
of weakness and chronic conditions like spinal muscular polio like illnesses. As oral polio vaccine is still used for
atrophy are not included here. vaccination, there is a very remote risk of vaccine derived
poliomyelitis.
Localization based on clinical signs (Table I)
Radicles and peripheral nerve
First step in the diagnosis is localizing the lesion.
Case history
LMN: Flaccid weakness with absent reflex is in favor of
LMN. After ascertaining that the motor weakness is due to Ten year old boy was admitted with weakness of lower
LMN, exact site of lesion like anterior horn cell, root, nerve, limb of five days and upper limb of two days duration.
myoneural junction or muscle is determined by verifying It started as knee buckling, difficulty climbing stairs and
the presence or absence of cranial nerve lesions, bladder getting up from sitting position. He had difficulty sipping
involvement, tendon reflexes and sensory involvement. water from a glass but was able to wear slippers and hold
Associated clinical features may give a clue to the the objects in hand. On 3rd day as he developed difficulty
etiological diagnosis (Table II).2 raising arm above shoulder and respiratory muscle
weakness. He had pain in the legs but no sensory loss.
Anterior horn cell disorders
There was no difficulty in urination. He had an upper
Case history respiratory tract infection 2 weeks ago.

Seven year old child was seen with history of fever, Comment: Pure proximal motor limb weakness with
severe myalgia, back pain and weakness of abduction of bifacial palsy and presence of respiratory muscle weakness
right shoulder. Examination revealed meningeal signs, mild is diagnostic of GBS. GBS presenting as painful limping
bulbar weakness, normal sensory and sparing of bladder may be confused as synovitis. Absent reflexes points
and bowel. CSF showed lymphocytic pleocytosis. towards GBS. Bifacial palsy can be missed as there is no
NCV/EMG suggested anterior horn cell disease. Serology facial deviation due to the symmetric weakness.
revealed enterovirus (type was not determined) on follow Difficulty puckering the lips or sipping, incomplete burying
up flail shoulder with severe wasting of deltoid was of eye lashes on tight eye closure are the clues.
persisting.
Guillain Barre syndrome (GBS)
Comment: Child had a poliomyelitis like presentation,
without isolation of any type of polio virus, but due to It is a progressive, near symmetrical weakness
another enterovirus. occurring in more than one limb with areflexia (Modified
Asbury’s criteria) (Box 1). The common subtypes are acute
Febrile illness, rapidly progressive asymmetric inflammatory demyelinating polyradiculoneuropathy
weakness, preserved sensory function, severe myalgia and (AIDP), acute motor axonal neuropathy (AMAN), acute
residual paralysis after 60 days are features of polio like motor sensory axonal neuropathy (AMSAN), Miller Fisher
illness.3,4 Enterovirus 71, Coxsackie, Echo and West Nile syndrome (MFS) and polyneuritis cranialis. The rare
viruses are the non polio viruses reported. 5 After the variants of GBS are acute pan-dysautonomia, acute sensory

Table I. Localization based on clinical signs

Anatomical level Clinical signs
Brain stem Altered consciousness, cranial nerve paralysis, Upper motor neuron (UMN) lesion signs
Spinal cord Bladder involvement, UMN lesion signs (below the level of lesion), plantar extensor
Anterior horn cells Lower motor neuron (LMN) type weakness, areflexia
Nerve root Lower motor neuron weakness, areflexia.
No sensory loss
Peripheral nerve Sensory loss, glove and stocking sensory involvement, loss of ankle reflex
Neuromuscular junction Diurnal variation, fluctuating weakness
Muscle LMN weakness but reflexes preserved
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Table II. Clues to diagnosis

Features Diagnosis
Fever Polio, Lyme disease
Myalgia or sensory symptoms GBS
Recent exanthem Lyme disease
Patch over tonsillar area, bull neck Diphtheria
Trauma/IM injection Traumatic neuropathy
Abdominal pain Porphyria, lead poisoning
Exposure to chemicals Arsenic, lead poisoning
Tick bite Tick paralysis
Ptosis, respiratory paralysis Snake bite, botulism
Dermatological manifestations - Edema, Gottron’s papules Dermatomyositis
Recurrent flaccid paralysis Periodic paralysis - channelopathies
Acute paralysis occurring in an ICU patient Critical illness neuropathy

ataxia with or without ophthalmoplegia, pharyngeal- diagnosis. The first changes in AIDP are delayed or absent
cervical-brachial weakness and facial diplegia with F and H responses, reflecting proximal demyelination.
paresthesias. Preceding infections associated with GBS Prolonged distal latencies, decreased conduction velocities
include Campylobacter jejuni, cytomegalovirus, Epstein- along with evidence of segmental demyelination,
Barr virus, mycoplasma pneumonia and HIV.6 (conduction block and temporal dispersion) are other
changes present in 50% of patients by 2 weeks and in 85%
MFS is characterized by ataxia, ophthalmoplegia and by 3 weeks.
areflexia without weakness. Anti-ganglioside GQ1B
antibodies are commonly detected in MFS. Brain stem The features raising doubt on the diagnosis of GBS
encephalitis also can have a similar presentation with ataxia are persistent asymmetry of weakness, presence of a
and ophthalmoplegia. However somnolence will be a sensory level, bowel/bladder involvement at onset and a
distinguishing feature. prominent CSF pleocytosis.
Electrophysiological abnormalities of GBS: Nerve Conditions that may have a presentation like GBS
conduction studies (NCV) are helpful in confirming the include neuropathy associated with HIV, Diphtheria, Lyme
Box 1. Guillain Barre syndrome - disease, porphyria and critical illness; polyneuropathy/
Diagnostic criteria myopathy and vasculitis syndromes.

 Presence of progressive weakness and areflexia Acute transverse myelitis (TM) (Box 2)

 Symmetrical involvement It presents as sudden limb weakness, bowel-bladder

and sensory disturbances and commonly occurs in toddlers
 Mild sensory involvement, cranial nerve and adolescents.
involvement, at least partial recovery
Postinfectious TM: Preceded by viral or bacterial
 Autonomic dysfunction infection. Viruses implicated are enteroviruses,
 Absence of fever coronavirus, coxsackie, cytomegalovirus, Epstein-Barr,
herpes-simplex, hepatitis A, HIV, influenza, measles,
 Cerebrospinal fluid features supporting the diagnosis rubella, varicella, and West Nile virus. Bacteriae include
are an increase in protein beyond the first week, cell mycoplasma pneumoniae, rickettsia, beta hemolytic
count < 10 (albumin-cytological dissociation) Streptococcus, borrelia, chlamydia and leptospira.

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Box 2. TM - Criteria for diagnosis Case report

 Sensory, motor, or autonomic dysfunction 13 year old boy presented with episodes of vomiting,
attributable to the spinal cord retching, hiccup and rapidly progressive weakness of both
lower limbs and left upper limb. He had urinary retention
 Absence of compressive cord lesion
and was frequently slipping to sleep. Sensory level was
 Bilateral symptoms and signs localized to T2 and tendon reflexes were sluggish with
 Definite sensory level extensor plantar.
 Spinal T2 MRI- hyperintense signals His MRI showed T2FLAIR hyperintensities involving
both grey and white matter of cerebral hemispheres and a
 Evidence of inflammation
large lesion on the floor of 4th ventricle. He had an extensive
 CSF pleocytosis, elevated IgG index, or gadolinium hyperintensity of spinal cord extending from C5 -T1.
enhancement on MRI His myelin oligodendrocyte glycoprotein (MOG) antibody
 Progression to nadir between 4 hours and 21 days6,7 titer was positive. This case exemplifies transverse myelitis
with area postrema syndrome. An aquaporin 4 negative
Post-vaccinal TM: May follow immunization for rabies, MOG positive neuromyelitis optica spectrum disorders
hepatitis B, influenza, Japanese encephalitis, diphtheria/ (NMOSD).
pertussis/tetanus, measles, mumps, rubella, pneumococcus, Comment: Though bladder symptoms, sensory level
polio, smallpox and varicella. localize the lesion to spinal cord, retching, vomiting and
hiccup point to area postrema involvement (The area
Acute flaccid paralysis with sensory level is a feature postrema is a highly vascular paired structure in the medulla
of TM. In children, mild sensory symptom like oblongata in the brainstem, in the caudal fourth ventricular
hyperaesthetic sites may be present which helps for floor. It is a critical homeostatic integration center for
localization. If legs are affected the sensory level is humoral and neural signals by means of its function as a
commonly at umbilicus or at the level of nipple. If the arms chemoreceptor trigger zone for vomiting in response to
are weak, look for sensory level at cervical region. emetic drugs).
Bowel and bladder involvement cause constipation and
urinary retention. Respiratory failure (intercostals or Traumatic neuropathy (TN)
diaphragmatic weakness) may occur with higher level Traumatic injury to peripheral nerves presents as focal
lesions. AFP. It includes injury to plexus, roots or peripheral nerves.
Variants of TM: Identifying TM variants will help in Nerve injuries can result from penetrating trauma
etiological diagnoses and thus treatment and prognoses (injections, falling on sharp objects), entrapment or from
traction injuries. Focal weakness is attributable to a single
1. Longitudinally extensive TM (LETM) - Lesion in >3 or multiple nerve distribution.
spinal segments associated with bilateral optic neuritis It is asymmetric. History of trauma is present near a
= neuromyelitis optica spectrum disorder. nerve or site of predilection. The common cause is an
2. Acute flaccid myelitis (AFM) - Like poliomyelitis they injection to gluteal or deltoid region. Commonly affected
have segmental LMN (AHC) and additional UMN nerves are common peroneal / sciatic (foot drop) or radial
lesion in the setting of other viral infections - (wrist drop). The knowledge of anatomy of nerve will help
e.g. enterovirus D68. These patients may recover with in identifying the specific nerve. The diagnosis is confirmed
residual wasting and weakness by nerve conduction studies. The prognosis depends on
severity of injury. Persistent, severe and refractory
3. Acute partial TM - Asymmetric extending one to two
neuropathic pain may be present along with weakness.
spinal segments.
Muscle
4. Acute complete TM - Symmetric, complete or near
complete manifestations Case report
An important differential of TM is acute spinal cord Eleven year old girl was admitted with 2 weeks history
infarct due to anterior spinal artery occlusion. 6 of painful weakness of upper and lower limbs. No sensory
Compressive myelopathy can present as acute syndrome. signs. Examination showed grade 3 power in proximal and
Both intramedullary and extramedullary compression like grade 4 in distal muscles. She had neck flexor weakness.
neuroblastoma can present acutely. Knee jerk and biceps jerk were very sluggish with easily
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Table III. Differential diagnosis of AFP

Features Poliomyelitis GBS Transverse myelitis Traumatic neuritis
Progression to 24-48 hrs Hours to days Hours to 4 days Hours to days
full paralysis
Fever onset High, always present No Present before paralysis No
at onset of paralysis
Distributing of Asymmetrical, Symmetrical, Symmetrical lower limbs Confined to nerve
weakness patchy distal Ascending distribution
Muscle tone Diminished Diminished Diminished in lower limbs Diminished
Deep Tendon Decreased or absent Absent Absent early, Decreased or absent
reflexes hyperreflexia late
Plantar reflex Absent/Flexor Absent/Flexor Extensor Absent/Flexor
Sensation Severe myalgia or Cramps, tingling, Anesthesia of lower limbs Pain in the gluteal region
backache no sensory hypo anesthesia with sensory level
changes of palms and soles
Cranial nerves Only in the presence Often present, Absent Absent
of bulbar or bulbo- affecting nerves
spinal involvement VII, IX, X, XI, XII
Respiratory Only in the presence In severe cases Sometimes Absent
insufficiency of bulbar and bulbo-
spinal involvement
CSFexamination Cell count raised, <10 leukocytes, Cell count: Normal/ Cell count: Normal
protein normal or high protein moderate lymphocytic Protein: Normal
slightly increased pleocytosis Protein:Normal/
protein slightly elevated
Bladder Absent Transient Present Never
dysfunction
EMG at 3 week Abnormal Normal Normal May be abnormal
NCV at 3 week Normal Abnormal Normal Abnormal
demyelination
/axonal
Sequelae at Severe, asymmetrical Symmetrical Diplegia, Moderate atrophy of
3 months atrophy atrophy of atrophy after years, affected limb
distal muscle
elicitable ankle jerk. Skin examination showed typical Polymyositis-dermatomyositis
features of dermatomyositis. CPK was found be raised.
AFP can be due to myositis also. Polymyositis-
Comment: Pure motor syndrome with proximal dermatomyositis can be suspected when there is a
involvement (grade 3 power, sluggish knee and biceps jerk) symmetric proximal muscle weakness without sensory
and high CPK indicated muscle disease. Acute onset and symptoms or signs and with preserved reflexes, neck
neck weakness suggested polymyositis and skin muscle weakness, muscle pain and raised CPK.
manifestations clinched the diagnosis of dermatomyositis. Acute myositis following viral infection also are not
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uncommon. Temporal relation with viral illness, high CPK Comment: Usage of certain drugs can worsen treated as
and rapid improvement are the features. Some children may well as naïve myasthenia gravis and can present as AFP.
require short course of steroid. Fluctuating weakness, simultaneous ocular and facial
muscle involvement and response to neostigmine are the
Case report diagnostic pointers. Bite marks and children playing in
dark, may suggest snake envenomation. Anti-snake venom
Four year old boy developed weakness of all four
and neostigmine will be life saving.
limbs and shallow breathing following a diarrheal illness.
He required respiratory support for a brief period. The important features of common causes of AFP are
Abdominal distension and poor bowel sounds were present. given in Table III.
Serum potassium was very low and ECG showed
depression of the ST segment, flat T wave with U wave. Investigations
Consciousness was preserved but tendon reflexes were
According to AFP surveillance, two stool samples
absent. Weakness rapidly improved with correction of
must be collected 24 to 48 hours apart in the first 14 days
hypokalemia.
following the onset of paralysis and to be sent to the
Comment: Syndrome of hypokalaemic paralysis accredited lab after following the surveillance protocol for
represents a heterogenous group of disorders characterised polio or related viral isolation (Fig.1). For diagnosis of
clinically by hypokalaemia and acute pure motor weakness. other disorders investigations such as blood counts, ESR,
Sporadic cases are associated with, renal disorders, peripheral smear, electrolytes (Ca,Mg,K) and CPK.
endocrinopathies and gastrointestinal potassium losses. Electrophysiological studies, NCV and EMG are done to
In adolescents hypokalemic periodic paralysis also can be evaluate types of GBS, myasthenia, muscle and nerve
a possibility. disorders. MRI of spinal cord and brain for distinguishing
various demyelinative disorders.
Neuromuscular junction disorders
CSF analysis
Case report
Raised CSF cell count is seen in transverse myelitis
Girl aged nine years was admitted in ICU with rapidly and infective myelitis viz. polio or enteroviral myelitis,
worsening limb weakness and severe respiratory paralysis varicella or herpes myelitis and rabies. Albumino-
who required ventilation for 5 days. This happened after a cytological dissociation (increased CSF protein with
bout of urinary tract infection, which was treated with normal cell count) is seen commonly in GBS but rarely in
ciprofloxacin. History of ptosis for 2 weeks occurring in post-diphtheritic polyneuropathy, transverse myelitis and
evening hours gave the diagnosis of myasthenic crisis. Froin’s syndrome (coexistence of xanthochromia,
Rapid deterioration was due to the usage of ciprofloxacin. high protein level and marked coagulation of cerebrospinal
She improved with IVIg and neostigmine treatment. fluid due to obstruction of CSF flow may indicate a spinal
Acetylcholine receptor (AChR) antibody was positive. tumor).

Fig.1. Time line for AFP evaluation

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Fig.2.Longitudinally extensive Transverse Fig.3a, b.T1 plain and T2 Lumbosacral spine

Myelitis – T2 hyperintensity extending from MRI in GBS
C5 - T7. Possibilities are NMO Spectrum
disorder or Enterovius myelitis
MRI8
TM: Up to 40% of cases have no findings on MRI.
The Diagnostic sign is T2 hyperintensity which most
commonly extends for 3-4 spinal segments with a variable
enhancement pattern.
Spinal cord infarct: It is characterized by an enlarged
spinal cord, which is hyperintense on T2 weighted images
and DWI. The signal intensity abnormality may be limited
to the central gray matter. The signal abnormality typically
extends over multiple vertebral body segments (Fig.2). The
vertebral body T2 hyperintensity may occasionally be seen
due to a concomitant infarction.
GBS: Typical findings in GBS are surface thickening and Fig.3C. Radiographic features of GBS
contrast enhancement on the conus medullaris and the nerve contrast T1 MRI lumbosacral. Typical
roots (anterior nerve roots) of the cauda equina. findings in GBS - nerve root thickening and
Contrast is must as non-contrast sequences are essentially enhancement surrounding the conus and the
normal (Fig.3a,b,c). cauda equina
of immobilization and prevention of nosocomial infections
MRI in inflammatory myositis may show increased are important considerations. The specific therapy depends
signal intensity in the quadriceps bilaterally (Fig.4) on the underlying etiology identified.
Management TM
General principles Intravenous methyl prednisolone (30 mg/kg up to
All children with AFP need meticulous supportive 1000 mg daily) for five days. Plasma exchange or,
care. Anticipation and identification of respiratory and intravenous cyclophosphamide (800 to 1200 mg/m 2
bulbar weakness is important. ICU admission will be administered as a single pulse dose.
required if airway obstruction, respiratory failure or GBS
significant autonomic disturbance is observed.
Management of shock due to reduced vascular tone, IVIG 400mg/kg/day for 5days in the presence of
management of autonomic instability and complications rapidly progressive weakness (Modified Hughes GBS
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Increased signal intensity in the

quadriceps bilaterally.

Fig.4. MRI in inflammatory myositis

Fig.5. Managment of GBS

PE max- Expiratory pressure; PI max- maximum inspiratory pressure VC vital capacity
AFP surveillance - Current status

disability scale), presence of respiratory or bulbar AFP surveillance - Current status

involvement (Fig.5). Ventilatory support may be required There has been a sharp fall in the incidence of
when there is respiratory failure. IVIG is not indicated if poliomyelitis across the world from 350,000 cases in
the degree of weakness is non-progressive and has been 125 countries in 1988 (year of starting Global Polio
present for more than 4weeks. Eradication Initiative (GPEI)) to 85 cases in 2 countries

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(Pakistan-69 and Afghanistan-16) as of 2019. This was Outbreak response immunization (ORI)
achieved by the active surveillance, immunization and
improvement in sanitation. India was declared polio-free The incubation period of the polio virus is 4-35 days
prior to weakness and all children 0-59 months of age in
on 27 March 2014, three polio free years after the last case
the affected area (around 500 children) where the child
was reported in January 2011 in West Bengal. As for world,
resided or visited in the incubation period are given active
type 2 virus serotype was declared globally eradicated in
immunization. The cases that are likely to be polio in the
2015 and Type 3 on 24th Oct 2019.
community are also actively investigated by the SIO and
Endgame Polio Strategy 2019-23 is the current in AFP cases with inadequate stool specimen, 60 day follow
strategy by the GPEI. The goals have three major up is done between 60 and 90 days.
components (Table IV).
The post certification strategy is also developed to
India has switched over to bivalent OPV in April 2016 maintain a polio free world. Its goals are
excluding the OPV 2 strain which is mainly responsible
for vaccine derived polio. Meanwhile, inactivated polio 1. Contain poliovirus sources by ensuring that they are
vaccine (IPV) was introduced in 2016 with two fractional controlled and removed
intradermal doses at 6 and 14 weeks along with bivalent 2. Withdraw OPV and immunize with IPV against
OPV. possible re-emergence of any polio virus
AFP surveillance is the strategy to screen for
circulating wild polio virus in the post-polio eradication 3. Defect and respond promptly to any polio virus
phase. The patients with AFP within the last 6 months reintroduction.
should be reported to the surveillance Medical Officer of The trivalent OPV which was in use till 2016 had a
WHO. The four steps of AFP surveillance are finding and highest sero conversion rates for type 2 and hence wild
reporting children with AFP, transport and analysis of stool polio virus type 2 was eradicated in 1999. Most cases of
sample, identify poliovirus in laboratory and determine the vaccine derived Polio Myelitis are due to OPV 2 and the
virus strain and origin. Within 48 hours of notification, a trivalent OPV was withdrawn and replaced with bivalent
trained medical officer investigates the case, proceeds with OPV since April 2016.
transportation of stool samples, outbreak response
immunizations done in the affected community. A 60 day Conclusion
follow up examination of the case is also done.
AFP is a complex clinical syndrome that requires
The non-polio AFP rate is an indicator of surveillance immediate and careful evaluation of the differential
sensitivity and should be equal to or more than 1: 1,00,000 diagnoses. Each case of AFP is an emergency from both
(background rate of AFP) according to National Polio clinical and public health perspective. The precise
Surveillance Project.9 knowledge of the etiology, underlying pathophysiologic
AFP surveillance is for detecting polio virus mechanisms and anatomic changes have profound
transmission. implications for prognosis and treatment. The role of

Table IV. Endgame Polio Strategy 2019-23 – Goals

Goal one: Eradication Interrupt transmission of all wild poliovirus (WPV)
Stop all circulating vaccine-derived poliovirus (cVDPV) outbreaks within 120 days of
detection and eliminate the risk of emergence of future VDPVs
Goal two: Integration Contribute to strengthening immunization and health systems to help achieve and sustain
polio eradication
Ensure sensitive poliovirus surveillance through integration with comprehensive vaccine
preventable disease (VPD) and communicable disease surveillance systems
Prepare for and respond to future outbreaks and emergencies
Goal three: Certification Certify eradication of WPV
& containment Contain all polioviruses
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infectious agents and immune processes as significant References

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and testing for the poliovirus. (editors). Bradley’s Neurology in Clinical Practice. 7 Ed.
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 Clinical features of polio must be taught to the flaccid paralysis afp › guidance › File, 14207, en.
younger residents as imported or vaccine associated Last accessed on January, 2020.
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enterovirus related TM, or NMO (neuromyelitis Schreiner T, Stence NV. MRI findings in children with acute
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 Rabies can present with features of GBS. and meta-analysis. Rev Med Virol 2019; e2082-2087.

CLIPPINGS

High-flow nasal cannula therapy as apneic oxygenation during endotracheal intubation in critically ill patients
in the intensive care unit: a systematic review and meta-analysis.
Hypoxemia, a frequently reported complication of intubation, is considered a predisposing factor for cardiac
arrest and death. Therefore, oxygenation during endotracheal intubation plays an important role in prolonging
the maintenance of acceptable oxygen saturation levels. Authors conducted asystematic review and meta-analysis
to assess the clinical efficacy of high-flow nasal cannula (HFNC) therapy as apneic oxygenation in critically ill
patients who require endotracheal intubation in the intensive care unit (ICU).Review included six randomized
controlled trials and a prospective study identified in PubMed, Embase, Cochrane Library, and the Web of
Science until August 18, 2019 involving 956 participants Risk ratio of severe hypoxemia decreased with increasing
baseline partial oxygen pressure (PaO2) to fraction of inspired oxygen (FiO2) ratio in the study group. In subgroup
analysis, HFNC significantly reduced the incidence of severe hypoxemia during endotracheal intubation in
patients with mild hypoxemia (PaO2/FiO2> 200mmHg. The authors concluded that HFNC was non inferior to
standard of care for oxygen delivery during endotracheal intubation and was associated with a significantly
shorter ICU stay. The beneficial effect of HFNC in reducing the incidence of severe hypoxemia was observed in
patients with mild hypoxemia.

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