GUILLAN BARRE

SYNDROME

SUBMITTED TO, SUBMITTED BY,

Bindu K Sankar Aswathy R C

Assistant Professor II yr MSc Nursing

Govt College of Nursing Govt College of Nursing

Thrissur Thrissur
GUILLAIN-BARRÉ SYNDROME

INTRODUCTION

Guillain-Barré syndrome (GBS), also known as infectious polyneuritis, is an uncommon

acute demyelinating polyneuropathy with a progressive, usually ascending flaccid paralysis.
Children are less often affected than adults, among children, those between ages 4 and 10
years have higher susceptibility. The male/female ratio is reported to be 1.5:1. Two peak time
periods have been identified with an increased incidence of GBS: late adolescence and young
adulthood. The incidence is also increased in pregnant and postpartum women.

Guillain-Barré syndrome (GBS) is an autoimmune disorder that is thought to be a post-

infectious polyneuropathy, involving mainly motor but also sensory and sometimes
autonomic nerves. This syndrome affects people of all ages and is not hereditary. Most
patients in the United States and Europe have a demyelinating neuropathy, but primarily
axonal degeneration is apparent in some forms of GBS, seen mainly in China, Mexico,
Bangladesh, and Japan.

Congenital GBS is rare yet may be seen in the neonatal period and consists of hypotonia,
weakness, and decreased or absent reflexes; maternal neuromuscular disease may or may not
be present. Diagnosis is established by the same criteria as in older children, but the
symptoms gradually subside over the first few months of life and disappear by 12 months.

DEFINITION

The Guillain-Barre-syndrome (GBS) is an acquired disorder of the peripheral nerves,

described as an autoimmune poliradiculoneuropathy, clinically characterized by the
progressive, symmetrical, usually ascending weakness, and diminished or absent reflexes,
variable sensitive involvement and increase in total protein in cerebrospinal fluid.

INCIDENCE

 The incidence in children is lower, with estimates between 0.4 and 1.3 cases per
100,000 per year.
 GBS is rare and affects approximately 1 person in 100.000 each year worldwide
(NINDS, 2010a).
 It affects all ages, including infants, It occurs moderately more often in males.
PREDISPOSING FACTORS

 Preceding a respiratory or gastrointestinal illness

 Viral infection like Haemophilus influenzae, herpes simplex virus, and mycoplasma
 Bacterial infection with Campylobacter jejuni
 Unknown
 The original infection might have caused only gastrointestinal (especially
Campylobacter jejuni, but also Helicobacter pylori), respiratory tract (especially
Mycoplasma pneumoniae), or systemic (Zika virus) symptoms.
 Consumption of undercooked poultry, unpasteurized milk, and contaminated water
are the main sources of gastrointestinal infections.
 West Nile virus also can mimic Guillain-Barré-like syndrome, but more often causes
motor neuron disease similar to poliomyelitis.
 GBS may follow administration of vaccines against rabies, influenza, and conjugated
meningococcal vaccine, particularly serogroup C.
 Other infectious precursors of GBS include mononucleosis. Lyme disease,
cytomegalovirus, and the Zika virus.

PATHOPHYSIOLOGY

GBS is an immune-mediated disease often associated with a number of viral or bacterial

infections or the administration of certain vaccines.

Onset of GBS symptoms usually occurs within 10 days of the primary infection.

Pathologic changes in spinal and cranial nerves consist of inflammation and edema with
rapid, segmented demyelination and com pression of nerve roots within the dural sheath.

Nerve conduction is impaired, producing ascending partial or complete paralysis of muscles

innervated by the involved nerves.

PHASES OF GBS

GBS has three phases:

1. Acute-

Starts when symptoms begin and continues until new symptoms stop appearing or
deterioration ceases; it may last as long as 4 weeks.

2. Plateau-

Symptoms remain constant without further deterioration; it may last from days to weeks.

3. Recovery-

Patient begins to improve and progress to optimal recovery; it usually lasts a few weeks to
months depending on the deficits incurred by the illness.
TYPES OF GBS

Subtypes of GBS include an

 Acute Inflammatory Demyelinating Polyradiculoneuropathy

 Acute Motor Axonal Neuropathy
 Acute Motor and Sensory Axonal Neuropathy
 Miller-Fisher syndrome

these are distinguished by findings on nerve conduction studies and an associated pattern of
antiganglioside antibodies.

Acute Inflammatory Demyelinating Polyradiculoneuropathy

 Accounts for 80-90 % of GBS cases.

 Characterized by an immune mediated attack on myelin with infiltration of
lymphocytes and macrophages with segmental stripping of myelin.
 Motor and sensory fibres are usually affected simultaneously, producing deficits
 Electrophysiology shows- slow nerve conductin velocity and prolonged F waves.

Acute Motor Axonal Neuropathy

 Axonal degeneration occurs by immune attack within 1-2 weeks after infection.
 Specific antibodies to axonal membranes of motor fibres attack the nodes of ranvier
 This in turn activates compliment and intrusion of macrophages into periaxonal space,
resulting in destruction of axons.
 Electrophysiology shows- reduction in muscle action potentials with relatively
preserved motor conduction velocity, normal sensory nerve action potentials and F
waves.

Acute Motor and Sensory Axonal Neuropathy

 It resembles AMAN except sensory nerves are also affected.

 This type is associated with a severe course and poor prognosis.

Localized forms of GBS also occur and include a pattern of facial diplegia with paresthesias
and a pattern of pharyngeal-cervical-brachial weakness.

Miller-Fisher syndrome:

Miller-Fisher syndrome is an uncommon GBS variant associated with acute external (and
occasionally internal) ophthalmoplegia, ataxia, and areflexia. The 6th cranial nerve is most
often involved in MFS. Although areflexia is seen in MFS. patients have no or only very mild
lower extremity weakness, compared with GBS. Distal paresthesias are common in MFS.
Urinary incontinence or retention is a complication in approximately 20% of cases but is
usually transient.
CLINICAL MANIFESTATIONS OF GUILLAIN-BARRE SYNDROME

INITIAL SYMPTOMS

 The onset of weakness usually follows a nonspecific gastrointestinal or respiratory

infection by approximately 10 days
 Radicular back pain and myalgia are common in the initial stages; affected children
can be very irritable.
 Weakness usually begins in the lower extremities and progressively involves the
trunk, the upper limbs, and finally the bulbar muscles, but weakness is sometimes
proximally prominent.
 Extraocular muscle involvement is rare, but many patients develop facial weakness.
In most patients, weakness is essentially symmetric.
 Weakness progresses over days or weeks, the clinical nadir occurring in less than 4
wk. Approximately 60% of children lose the ability to walk at some point in their
illness; a small proportion progress to flaccid tetraplegia. The maximal severity of
weakness is reached by 4 wk after onset.
 Muscle tenderness
 Paresthesia and cramps (sometimes) followed by weakness
 Proximal symmetric muscle weakness
 Ascending paralysis from lower extremities
 Frequently involves muscles of trunk and upper extremities and those supplied by
cranial nerves (especially facial)
 Flaccid paralysis with loss of reflexes
 May involve facial, labial, lingual, pharyngeal, and laryngeal muscles
 Intercostal and phrenic nerves: Breathlessness in vocalizations
 Shallow, irregular respirations
 Cranial nerve dysfunction, with facial nerve paralysis, dysphagia, and inadequate
cough, gag, and swallow reflexes. If this occurs, respiratory function will be impaired.
 Respiratory failure resulting from the progressive motor paralysis of the intercostal
and phrenic nerves.
 Respiratory failure may occur in 15% to 25% of children with GBS.
 Bulbar involvement occurs in about 50% of cases and can result in respiratory
insufficiency

OTHER MANIFESTATIONS

 Tendon reflexes depressed or absent

 Variable degrees of sensory impairment
 Muscle tenderness or sensitivity to slight pressure
 Urinary incontinence or retention and constipation
 Autonomic instability, including blood pressure fluctuations, cardiac arrhythmias,
postural hypotension.
  Neuromuscular impairment (bilateral ascending weakness or paralysis) usually
progresses upward from the feet to the head. (As healing takes place, neuromuscular
function returns gradually in reverse order-head to feet.)
 Dysphagia and facial weakness can be signs of impending respiratory failure, interfere
with saliva control and swallowing, and increase the risk of aspiration.
 Vocal cord paralysis may cause dyspnea or a hoarse voice. Severe bulbar and
respiratory muscle involvement can lead to death if GBS is not recognized and
treated.

DIFFERENTIAL DIAGNOSIS

Spinal cord lesions

 Acute transverse myelitis- Transverse myelitis is an inflammation of both sides of one

section of the spinal cord. This neurological disorder often damages the insulating
material covering nerve cell fibers (myelin).Transverse myelitis interrupts the
messages that the spinal cord nerves send throughout the body. This can cause pain,
muscle weakness, paralysis, sensory problems, or bladder and bowel dysfunction

 Epidural abscess - Epidural abscess is a rare disorder caused by infection in the area
between the bones of the skull, or spine, and the membranes covering the brain and
spinal cord (meninges). This infection is called an intracranial epidural abscess if it is
inside the skull area. It is called a spinal epidural abscess if it is found in the spine
area. Most are located in the spine.
 Tumors
 Poliomyelitis
 Enteroviruses
 Acute flaccid myelitis - Acute flaccid myelitis (AFM) is a neurologic condition. It
affects the nervous system, specifically the area of the spinal cord called gray matter,
which causes the muscles and reflexes in the body to become weak.
 Hopkins syndrome- Hopkins syndrome (HS) is a rare disorder presenting with acute
flaccid paralysis of the limbs following an asthma attack.
 Vascular malformations
 Cord infarction
 Fibro cartilaginous embolism
 Cord compression from tumors
  Acute disseminated encephalomyelitis-It is a neurological, immune-mediated disorder
in which widespread inflammation of the brain and spinal cord damages white matter.
Damage to the myelin sheath affects the nerve’s ability to transmit information and
potentially can cause a wide range of neurological symptoms.
 Bickerstaff brainstem encephalitis- It is a rare post-infectious neurological disease
characterized by the association of external ophthalmoplegia, ataxia, lower limb
arreflexia, extensor plantar response and disturbance of consciousness .
 Anterior spinal artery syndrome- It is syndrome caused by ischemia of the anterior
spinal artery, resulting in loss of function of the anterior two-thirds of the spinal cord.
 matory demyelinating polyneuritis (acute onset)

DIAGNOSIS
 CSF analysis:

CSF study shows a characteristic albumin-cytological dissociation in majority of the patients

within 2 to 3 weeks of illness. There is increased protein level (more than 45 mg/dL), but cell
count is usually normal or slightly raised. Bacterial cultures are negative, whereas viral
studies rarely isolate specific viruses. The dissociation between high CSF protein and a lack
of cellular response (cyto albuminologic dissociation) in a patient with an acute or subacute
polyneuropathy is essentially diagnostic of GBS. These findings may not be apparent in the
first week after the onset of symptoms.

 Electrophysiology:

Electromyography in GB syndrome shows acute denervation of muscles. Motor nerve

conduction velocities and sensory conduction times are found slow.Nerve conduction studies
and electromyography are sensitive to early signs of peripheral nerve inflammation in GBS.
Motor and sensory nerve conduction velocities are reduced to a variable extent, reflecting the
patchy nature of nerve involvement in this disorder, which is also reflected in the presence of
focal conduction block and dispersed responses. Serum creatine kinase levels may be mildly
elevated or normal. Serum antiganglioside antibodies against GM, and GD, are sometimes
elevated in GBS, particularly in cases with primarily axonal rather than demyelinating
neuropathy, suggesting that they might play a role in disease propagation and/or recovery in
some cases .

 MRI spine

On magnetic resonance imaging (MRI) of the spinal cord in GBS, typical findings include
thickening of the cauda equina and intrathecal nerve roots with gadolinium enhancement.
  Sural nerve biopsy

Shows segmental demyelination, focal inflammation, and Wallerian degeneration, but is

almost never required for diagnosis.

 Serologic testing for Campylobacter and Helicobacter infections

Helps establish causation if results are positive but does not alter treatment. Stool cultures are
rarely positive because the infection is self-limited and only occurs for about 3 days, and the
neuropathy follows the acute gastroenteritis.

DIAGNOSTIC CRITERIA FOR GUILLAIN-BARRÉ SYNDROME

Features needed for diagnosis of Guillain-Barre Syndrome in clinical practice

 Progressive weakness in legs and arms (sometimes initially only in legs).

 Areflexia (or decreased tendon reflexes) in weak limbs,

Additional symptoms

 Progressive phase lasts days to 4 wk (often 2 wk).

 Relative symmetry.
 Mild sensory symptoms or signs (not present in acute motor axonal neuropathy).
 Cranial nerve involvement, especially bilateral weakness of facial muscles.
 Autonomic dysfunction.
 Pain (common).

Features that should raise doubt about the diagnosis

 CSF: increased number of mononuclear cells or polymorphonuclear cells (>50

cells/μL).
 Severe pulmonary dysfunction with little or no limb weakness at onset.
 Severe sensory signs with little or no weakness at onset.
 Bladder or bowel dysfunction at onset.
 Fever at onset.
 Sharp spinal cord sensory level.
 Marked, persistent asymmetry of weakness. Persistent bladder or bowel dysfunction.
 Slow progression of weakness and without respiratory involvement (consider
subacute inflammatory demyelinating polyneuropathy or acute-onset chronic
inflammatory demyelinating polyneuropathy).

Nerve conduction studies

 Can be helpful in clinical practice but are generally not required to diagnose Guillain-
Barre syndrome.
  Essential for classification of Guillain-Barre syndrome as acute inflammatory
demyelinating polyneuropathy or acute motor axonal generally not required to
neuropathy.
 Acute inflammatory demyelinating polyneuropathy, features of demyelination
(decreased motor nerve conduction velocity, prolonged distal motor latency, increased
F-wave latency, conduction blocks, and temporal dispersion).
 Acute motor axonal neuropathy: no features of demyelination lore demyelinating
feature in one nerve, if distal CMAP amplitude is e than 10% LLN, can be found;
distal CMAP amplitude less than 80% LLN in at least two nerves. Transient motor
nerve conduction block might be present.

PREVENTION OF COMPLICATIONS

Throughout the recovery phase, special emphasis is placed on prevention of

complications, including proper postural alignment, frequent change of position,
assessment of skin at pressure points, and passive exercises.
Respiratory care, should intubation be required, requires close monitoring of
oxygenation status, usually by pulse oximetry and arterial blood gases; maintenance
of an open airway with suctioning; and postural changes to prevent pneumonia.
Children with oral and pharyngeal involvement may be fed via a nasogastric tube to
ensure adequate feeding.
Immobilization, which occurs with GBS, decreases gastrointestinal function; therefore
attention to problems such as decreased gastric emptying and constipation requires
nursing assessment and appropriate collaborative interventions.
Prevention of deep vein thrombosis is accomplished with antiembolism devices,
administration of a low-molecular weight heparin, and early mobilization and
ambulation.
Sensory impairment and paralysis in the lower extremities makes the child susceptible
to skin breakdown; therefore attention should be given to meticulous skin care.

Parents are en couraged to talk to the child and make eye and physical contact as much as
possible to reassure the child during the illness. Psychosocial care of the child with GBS
focuses on dealing with the child's anxiety and fear related to the disease itself and the
unknown prognosis. In addition, the child's parents are allowed to express feelings and are
encouraged to involved in the child's daily care.

Pain management is crucial in the care of children with GBS. Although neuromuscular
impairment may make pain perception more difficult to accurately evaluate, objective pain
scales should be used.

Physical therapy is limited to passive range-of-motion exercises during the evolving phase of
the disease. Later, as the disease stabilizes and recovery begins, an active physical ther apy
program is implemented to prevent contracture deformities and facilitate muscle recovery.
This may include active exercise, gait training, and bracing.
Throughout the course of the illness, support of the child and parents is paramount. The usual
rapidity of the paralysis and the long period of recovery greatly tax the emotional re serves of
all family members. The parents and child benefit from repeated reassurance that recovery is
occurring and from realistic information regarding the possibility of permanent disability. In
the event of a residual disability, the family needs assistance in accepting and adjusting to the
loss of function. The GBS/CIDP Foundation International is a nonprofit organization devoted
to support, education, and research. It provides support to families from recovered persons,
publishes informational literature and a newsletter, and maintains a list of practitioners
experienced with the disease.

TREATMENT

In early stages of this acute disease should be admitted to the hospital for observation because
the ascending paralysis can rapidly involve respiratory muscles and cause respiratory failure
and autonomic instability.

The respiratory effort (measured by bedside testing or spirometry) must be monitored for
changes predicting an onset of hypoventilation and respiratory failure.

Patients with milder weakness and slow progression may be treated expectantly, with observa
tion for stabilization and spontaneous remission.

Children with relapsing or slowly progressive weakness often need months to years of
therapy, but most eventually achieve a sustained remission. The outcome is generally good,
but some children have permanent deficits.

CSF FILTRATION

 CSF filtration has been used in patients with GBS with some success
 CSF is removed, filtered, and replaced into the patient.
 This process presumably removes toxins and bacteria; however, further studies are
needed to evaluate this treatment modality

PHARMACOLOGICAL TREATMENT

 Intravenous immunoglobin
Severe or rapidly progressive muscle weakness is treated with intravenous
immunoglobulin (IVIG); common protocols include IVIG 0.4 g/kg/day for 5
consecutive days or 1g/kg/day for 2 days.

 Plasma exchange
Plasma exchange started within 2-4 weeks of onset of illness. If not responding in
initial treatment with IVIG, second course may be helpful. Plasmapheresis and/or
immunosuppressive drugs are alternatives if IVIG is ineffective.
Steroids are not effective for weakness but may help with pain. Supportive care, such as
respiratory support, prevention of pressure sores, nutritional support, pain management,
prevention of deep vein thrombosis, and treatment of secondary bacterial infections is
important.

Medications that may be administered during the acute phase include a

 low-molecular-weight heparin to prevent deep vein thrombosis

 mild laxative or stool softener to prevent constipation
 pain medication such as acetaminophen, and
 histamine-antagonist to prevent stress ulcer formation.

SUPPORTIVE MEASURES

 Prevention of secondary infection and pressure sore

 Maintenance of nutrition and hydration
 Physiotherapy and good nursing care are important supportive measure.
 The patient may need specialized management is intensive care unit (ICU)-
Cardiorespiratory monitoring, pain management, care of bladder and bowel and
prevention of thrombosis.

PROGNOSIS

 GBS is usually a monophasic illness; spontaneous recovery begins within 2-3 wk but
can take months.
 Therapy with IVIG hastens recovery but not does alter the long-term outcome.
 As many as 60% become non ambulant during their illness, but most eventually
regain full strength.
 A minority has some residual weakness, most often of the ankle dor siflexors. Clinical
features predicting a severe course and slow (possibly incomplete) recovery include
cranial nerve involvement, the need for ventilatory support, and maximum disability
at the time of presentation.
 The tendon reflexes are usually the last function to recover. Improvement usually
follows a gradient opposite the direction of involvement, with bulbar function
recovering first and lower extremity weakness resolving last. Bulbar and respiratory
muscle involvement can lead to death if the syndrome is not recognized and treated.
 In majority of the patients, the disease is self-limiting. In acute stage, symptomatic
and supportive management are important and should be done same as poliomyelitis.
Treatment of GBS is primarily supportive. In the acute phase patients are hospitalized
because respiratory and pharyngeal involvement may require assisted ventilation,
sometimes with a temporary tracheotomy.
  Assisted ventilation and tracheostomy may be needed in some patients with
respiratory paralysis. Corticosteroid therapy, plasma exchange therapy and
plasmapheresis can be provided.
 Plasmapheresis has been shown to decrease the length of recovery in patients with
severe GBS yet is expensive, and side effects include hypotension, fever, bleeding
disorders, chills, urticaria, and bradycardia. Corticosteroids alone did not decrease the
symptoms or shorten the duration of the disease.

NURSING CARE MANAGEMENT

Nursing care is essentially supportive and is the same as that required for the child with
immobilization and respiratory depression. The emphasis of care is on close observation to
assess the extent of paralysis and on prevention of complications, including autonomic
dysfunction (hypertension, orthostatic hypotension, syndrome of inappropriate antidiuretic
hormone secretion, life-threatening dysrhythmias), respiratory dysfunction, fear and anxiety,
and pain management.

ASSESSMENT

A complete history and physical examination are important to deter mine the presence
of an antecedent viral illness and establish baseline clinical status.

Special emphasis is given to evaluating the respiratory and neurologic systems.

Respiratory assessment should be done hourly or more frequently in some cases
because of the risk of respiratory compromise and the need for prompt action,
including intubation and ventilator support, if the child's respiratory status
deteriorates.

Major assessment parameters include

 respiratory rate
 chest excursion
 energy expended to breathe
 breath sounds.

Pulse oximetry assesses the effectiveness of gas exchange.

Daily pulmonary function testing may be ordered. A thorough neurologic assessment

is generally performed every 1 to 2 hours, though this may be done more frequently
depending on the child's clinical condition.

Neurologic parameters to address include cranial nerve function, motor capabilities,

sensory perception, and deep tendon reflexes.
During the acute phase of GBS the child's condition should be carefully observed for
possible difficulty in swallowing and respiratory involvement.
 The child's respiratory function is closely monitored, and oxygen source, appropriate-
sized resuscitation bag and mask, endotracheal intubation and suctioning equipment,
tracheotomy tray, and vasoconstrictor drugs are kept available.
Vital signs, including neurologic signs and level of consciousness, are monitored
frequently.

NURSING CARE OF THE CHILD WITH GUILLAIN-BARRÉ SYNDROME

Nursing Diagnosis and Planning

The following nursing diagnoses and expected outcomes may be appropriate after assessment
of the child with GBS:

1.Ineffective Breathing Pattern related to neuromuscular impairment.

Expected Outcome. The child will remain free from respiratory distress, as evidenced by
clear bilateral breath sounds, good chest expansion, and normal tidal volume.

2.Decreased Cardiac Output related to autonomic instability.

Expected Outcome. The child will maintain cardiac output, as evi denced by brisk capillary
refill, normal urine output, good pulses in all extremities, and no arrhythmias.

3.Risk for Impaired Skin Integrity related to immobility with paralysis. Expected Outcome.
The child will maintain skin integrity, as evidenced by absence of skin breakdown or pressure
ulcers.

4.Impaired Verbal Communication related to neuromuscular impairment.

Expected Outcome. The child will maintain the ability to communicate, as evidenced by
demonstration of new ways to communicate with available muscles, such as eye blinks or eye
movements.

5.Impaired Urinary Elimination related to paralysis.

Expected Outcome. The child will have acceptable urinary elimina tion, as evidenced by an
empty bladder, no urinary tract infection or distention of the abdomen, and urine output
within normal limits for age .
6.Anxiety related to increasing ascending paralysis.

Expected Outcome. The child will display decreased anxiety, as evidenced by an ability to
interact calmly with parents and health care providers and have decreased fretful periods and
increased restful periods.

7.Deficient Knowledge related to unfamiliarity with disease progression, treatment, and home
care.

Expected Outcome. The child and parents will have increased knowledge of the disease and
treatment, as evidenced by an ability to make plans about discharge care and discuss the
illness and possible complications.

8.Interrupted Family Processes related to having a child with a prolonged illness. Expected
Outcome. The parents will use coping strategies to adjust to their child's illness, as evidenced
by discussing support systems and changes in the family.

Interventions

 The goals of nursing care for the child with GBS are to achieve optimal neurologic
function with an emphasis on maintaining independence in activities of daily living
and to facilitate a recovery without complications.
 Treatment of GBS is largely supportive, with a focus on assessing and monitoring the
child's clinical status and preventing or minimizing complications.
 The nurse must be able to recognize any change in the child's condition and intervene
in a timely and effective manner.
 The nurse must anticipate possible deterioration in the child's respiratory status
because of progressive muscle weakness leading to flaccidity.
 Resuscitation and ventilatory support may be urgently needed; appropriate emergency
equipment and personnel should be available.
 Equipment, such as a bag-valve-mask device, oxygen, suction, endotracheal tubes
with stylets, and a laryngoscope with a variety of blades, should be at the bedside for
immediate access. To prevent infec tion, chest physiotherapy should be performed
every 2 to 4 hours.
 Interruption in the autonomic nervous system reflexes can cause circulatory changes,
resulting in arrhythmias, hypotension, dizziness, and night sweats.
 Ear detection of neurologic changes is made by serial assessments, and prompt action
should be taken to correct problems and prevent complications.
 The child with GBS is at an increased risk for developing complications associated
with immobility.
 Maintaining skin integrity is a priority. Turning, repositioning, passive range of
motion, and monitoring pressure points are performed by the nurse at least every 2
hours. Use of special mattresses and managing incontinence will help prevent skin
breakdown.
  To prevent contractures, daily physical and occupational therapy are included in the
child's treatment plan. Range of motion, active exercises, correct alignment, and
application of splints and braces are all part of the child's daily care.
 The risk of pulmonary embolus as a result of deep vein thrombosis is always a threat.
Frequent turning and repositioning, with special attention to positioning the child's
legs to alleviate pressure on the dorsal aspect of the knees, are essential.
 Anticoagulant therapy may be initiated; if so, the nurse should monitor clotting times
and watch for any signs of bleeding, As cranial nerve function is altered and
interference with gag and swallow occurs, nutrition becomes a vitally important issue.
 Adequate caloric intake is essential to prevent catabolism. Alternative methods of
providing nutrition must be used. The physician may order nasogastric,
nasojejunostomy, or gastrostomy feedings. The nurse monitors the type and amount
of feeding, tube placement and patency, tolerance of feedings (residuals, abdominal
distention, stools), and weight gain. Total parenteral nutrition is provided the child
during the acute phase of the illness or if alternative methods of nutritional support are
not tolerated. The progression of GBS is unpredictable, the loss of function is
frightening, and the recovery time varies from months to years.

RELATED RESEARCH STUDY

A study to identify treatment response in relation to the short-term outcomes of GBS

Retrospective study included children diagnosed with GBS in the Pediatric Neurology
Department of the Children's Hospital of Hebei Province from 2016 to 2020. According to
the rate of response from the standard intravenous immunoglobulin (IVIg) treatment, patients
were divided into two groups: rapid-response GBS (initial response within 7 days) and slow-
response (initial response within 8–30 days). The GBS disability score (Hughes Functional
Grading Scale) was used to assess the children's functional disability at nadir, 1 month, and 6
months after onset.
Results: Among the 36 children included in the study, 18 (50%) and 18 (50%) were rapid
and slow responders, respectively. Time from IVIg treatment to the initial response was
significantly shorter in the rapid-response group (5 [3–6.25] days vs. 10.5[8.75–15] days in
slow-response GBS, p < 0.001). Hughes score at 1 month was worse than the rapid
responders (Fisher's exact test, p = 0.006). Survival analysis (Kaplan–Meier) with respect to
regaining the ability to walk independently (Hughes Functional Grading Scale of 2) within 1
month after onset was significantly different among the two groups (log-rank test for
trend, p = 0.024). The abnormal levels of cerebral spinal fluid proteins and autonomic
dysfunction were more frequent in the slow-response group than those in the rapid group (p <
0.05).
Conclusion: The rate of response to IVIg treatment was correlated with short-term outcomes
in children with GBS and had predictive value for prognosis. The role of patient's initial
responses to treatment could be significantly valuable in developing more effective and
efficient treatment options.

REFERENCE

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2020.Page no. 3335-3340.

2. PSN Menon, MKC Nair. IAP textbook of pediatrics.7th Edition. Page no: 620-629.

3.Marylyn, David Wilson. Wong’s essentials of pediatric nursing.8 th edition.Elsevier

Publishers.