SEMINAR

ON

GULLAIN - BARRE SYNDROME

SUBMITTED TO, SUBMITTED BY,

Ms. M. Benita Devi Farida Parbin

Professor cum principal 1st year m.sc nursing

RINPS RINPS
INTRODUCTION:
Guillain-Barre syndrome also known as Landry – Guillain – Barre – Strohl syndrome,
polyneuropathy, ascending polyneuropathic paralysis . It affects the peripheral nervous
system and results in loss of myelin ( segmental demyelination ) , edema and inflammation
of the affected nerves , causing loss of neurotransmission to the periphery.

INCIDENCE:

 The syndrome affects males 1.5 times more frequently than females and is typically
seen in adults, although it is observed in all age groups.
 Worldwide the incidence has varied from 1 to 4 per 100,000 of population every
year.
 With adequate supportive care, 85% to 95% of patients recover completely from this
disorder.

DEFINITION:
Guillain-Barre syndrome is a disorder that causes damage to the peripheral nerves. The nerve
injury often causes muscle weakness, often does cause paralysis and sensitivity problems,
including pain, tingling or numbness.

CAUSES:

 Compylobacter jejuni
 Influenza
 Cytomegalovirus
 Epstein – Barr virus
 HIV or AIDS.
 Preceding vaccination
 Bacterial infection
 Viral infection
 Protozoan infection
 Surgeries
 Blood Transfusion and Transplantation
 Preceding heat stroke
 Several drugs – anaesthesia, analgesic .
ANATOMY AND PHYSIOLOGY:

Neuron:
 A typical neuron possesses a cell body (often called the soma), dendrites, and an
axon.
 Dendrites are thin structures that arise from the cell body, a complex "dendritic tree".
 An axon is a special cellular extension that arises from the cell body at a site called
the axon hillock .
 The cell body of a neuron frequently gives rise to multiple dendrites, but never to
more than one axon, although the axon may branch hundreds of times before it
terminates. At the majority of synapses, signals are sent from the axon of one neuron
to a dendrite of another. Exceptions to these rules: neurons that lack dendrites,
neurons that have no axon, synapses that connect an axon to another axon or a
dendrite to another dendrite, etc.
DEMYELINATION:

 A demyelinating disease is any disease of the nervous system in which the myelin
sheath of neurons is damaged.

 This impairs the conduction of signals in the affected nerves, causing impairment in
sensation, movement, cognition, or other functions depending on which nerves are
involved.
 PATHOPHYSIOLOGY:

Contamination of water

Pathogen (C. jejuni) +

Immature antigen presenting Innate immune response
cell

 MHC (Mature, differentiated antigen

presenting cell) migrates to lymph nodes. Pathogen & host have identical amino acid
 Activate CD4T cells; in the same time sequences, antigens in its capsule are shared
activate B cells with nerves
 Cell mediated + humoral immunity
response

Antibodies produce Molecular mimicry

Activation of the complement system
and phagocytosis of bacteria

Antibodies that produced cross react with

myelin, Lymphocytes and macrophages
circulate in blood & find myelin.

Lymphocytic infiltration of spinal roots

Defects the propagation of electrical & peripheral nerves. Macrophage –
nerve impulses, with eventual conduction mediated , multifocal stripping of
block myelin & axonal damage

Guillain – Barre syndrome

CLINICAL FEATURES:
It is a heterogeneous condition with symptoms ranging from mild to severe. It is usually
develop 1 to 3 weeks after an upper respiratory or gastrointestinal infection.

 Weakness of the lower extremities(evolving more or less symmetrically)

 Distal muscles are more severely affected .
 Paresthesia (numbness and tingling)
 Hypotonia (reduced muscle tone)
 Areflexia (lack of reflexes)
 Orthostatic hypotension.
 Hypertension
 Abnormal vagal responses like – bradycardia, heart block, asystole.
 Bowel and bladder dysfunction
 Facial flushing
 Diaphoresis
 Patients may also have syndrome of inappropriate antidiuretic hormone secretion
 Facial weakness , extra ocular eye movement difficulties, dysphagia and paresthesia
of face.
 Pain can be categorized as muscular aches and cramps and hyperesthesia’s . Pain
appears to be worse at night.

TYPES OF GUILLAIN BARRE SYNDROME:

I. Acute Inflammatory Demyelinating Polyneuropathy(AIDP):

 Prevalent in western countries (90% of the GBS cases)
 Adults are affected more than the children.
 First attack appears directed against a component of Schwann cell cause of flaccid
paralysis and sensory disturbances is the block of conduction, whereas axonal
connection remains intact.
 Recovery is most often rapid as remyelination occurs.
 In the severe forms of AIDP ,when axonal damage occurs , the rate of recovery is
slower and the degree of residual disability greater.

II. Acute Motor Axonal Neuropathy (AMAN):

 Prevalent in China & Mexico with seasonal prevalence.
 Children and young are affected more than adults.
 First attack appears directed against the axolemma and nodes of ranvier.
 Axonal damage is the prominent pathological alteration.
  Recovery takes place when axon regeneration is complete and it is rapid when lesion
is localized .

III. Acute Motor-Sensory Axonal Neuropathy(AMSAN):

 It is very rare and Closely related to AMAN.
 Adults are mostly affected .
 First attack is directed at motor nodes of ranvier, but also affects Sensory nerve and
roots.
 Here axonal damage is severe .
 Recovery is slow and often incomplete.

IV. Miller-Fisher Syndrome:

 Mosty adults ,young and children are affected.
 It involves peripheral nervous system and central nervous system structures.
 Its pathological features resemble that of acute inflammatory demyelinating
polyneuropathy (AIDP).
 Characterized by rapidly evolving of opthalmoplegia (often with pupillary paralysis),
ataxia, tendon areflexia (without weakness).
 Recovery is rapid.

COMPLICATION:
 The most serious complication of this syndrome is respiratory failure :
It occurs as the paralysis progresses to the nerves that innervate the thoracic area.
Constant monitoring of the respiratory system by checking respiratory rate and depth,
forced vital capacity .
 Respiratory tract infection, urinary tract infection.
 Paralytic ileus.
 Muscle atrophy.
 Deep vein thrombosis
 Pulmonary emboli.
INVESTIGATION:

 Lumber puncture – cerebrospinal fluid (CSF).

 Elevation of CSF protein (more than twice upper limit of normal)
 Cell content of CSF is normal.
 Glucose level normal
 Bacterial and viral culture is negative.
 Electromyography
 Motor nerve conduction velocities are greatly reduced and sensory nerve
conduction time is often slow
 Serum creatine kinase
 Elevated or normal.
 Muscle biopsy
 Appear normal in early stages
 Show evidences of denervation atrophy in chronic stages.
 Sural nerve biopsy
 Segmental demyelination, focal inflammation
 Serologic testing for campylobacter infection.

TREATMENT:
 Patients with early stages of this acute disease :
Should be admitted to the hospital for observation because the ascending paralysis
may rapidly involve respiratory muscles during the next 24 hour.
 Patients with slow progression:
May simply be observed for stabilization and spontaneous remission without
treatment .
 Patients with rapidly progressive ascending paralysis:
 Intravenous immunoglobulin should be administered:
Immunoglobulin containing healthy antibodies from blood donors is given
intravenously. High doses of immunoglobulin can block damaging antibodies
that may contribute to Gullain – Barre syndrome.

 Plasmapheresis, steroids or immunosuppressive :

In plasmapheresis or plasma exchange therapy, the liquid plasma is removed
and separated from blood cells after that blood cells are put back to body,
which helps to manufacture more plasma to make up for what was removed .

NUTRITTIONAL THERAPY:

 Mild dysphagia can be managed by placing the patient in an upright position and
flexing the head forward during feeding .
 For severe dysphagia tube feeding may be required.
  Patients who experience paralytic ileus or intestinal obstruction may require
parenteral nutrition.

PHYSIOTHERAPY MANAGEMENT:

i. Respiratory care:
 If patient is on ventilator , suctioning can be done (if required)
 Encourage the patient to do exercise
-Diaphragmatic breathing
-Incentive spirometery
-Glossophayrengeal breathing
-Chest mobilization exercise.
ii. Prevention from decubitus ulcer:
 By Repositioning.
 By Devices (e.g. pneumatic gloves)
 By providing nutritious food.

iii. Prevention from deep vein thrombosis:

 Begin ambulation as soon as possible
 Anticoagulant as a prophylactic treatment.
 Active pumping exercise
 Keep lower extremities elevated.

iv. Prevention from contractures:

 Generalized range of motion exercise.
 Spinal movements should be included e.g.
a. Double knee-and-hip flexion,
b. Knee rolling and
c. Neck movements with due care of tracheal tubes.

v. Reducing the risk of hypotension:

 Ensuring that turning is gentle
 Avoiding any intervention if CVP is below
 Risk of bradycardia is reduced by oxygenation before and after suction
NURSING MANAGEMENT :
1) Ineffective breathing pattern related to ascending paralysis as evidenced by altered
chest expansion.

Intervention:
 Assess frequency , symmetry and depth of breathing .
 Observed for breathing and evaluate skin color, temperature and capillary refill.
 Observe for signs of respiratory fatigue such as shortness of breath, decreased
attention span and impaired cough.
 Auscultate lung sounds for any changes and notifies the physician immediately.
 Assess oxygen saturation and review client’s arterial bl;ood gases results.
 Keep the head of the bed elevated .

2) Acute pain related to nerve injury as evidenced by Guarding behaviour and autonomic
responses of diaphoresis.

Intervention:
 Assess level of pain and ability to engage in activities.
 Administer analgesics based on pain assessment and as per physician order.
 Provide support to extremities and maintain clean, comfortable bed.
 Reposition client every 2 hours, use good postural alignment, assist with passive
ROM.
 Apply a moist warm compress to painful areas as needed. 

3) Impaired physical mobility related to neuromuscular impairment as evidenced by

decreased muscle strength and control.

Intervention:
 Assess motor strength or functional level of mobility.
 Place the client in a position of comfort. Provide frequent position changes as
tolerated.
 Monitor nutritional needs as they associate with immobility.
 Provide padding to bony prominences such as elbow and heels.
 Perform active, passive and isotonic range of motion exercises as appropriate.
 Assist client and their families to establish goals in participation with activities,
exercise and position changes.
  Consider the need for home assistance (e.g., physical therapy and occupational
therapy).
 Evaluate the need for assistive devices and provide a safe environment e.g., bed in
low position and side rails up.

4) Impaired urinary elimination related to neuromuscular impairment as evidenced by

urinary retention.

Intervention:
 Assess progressive degree of paralysis and effect on urinary elimination.
 Monitor intake and output every 4 to 8 hours
and palpate bladder every 2 hours; assess for cloudy, foul-
smelling urine.
 If needed, insert an indwelling urinary catheter to maintain elimination.
 Instruct the family members to report any reduction or absence of urinary
elimination.
 Instruct family members to maintain fluid intake and monitor output in connection
to intake.

5) Anxiety related to Change in health status and threat to self-concept as evidenced by

Increased apprehension as the condition worsens and paralysis spreads.

Intervention:
 Assess source and level of anxiety, how anxiety is manifested and need for
information that will relieve it.
 Therapeutically communicate with family members and client and answer
questions in a calm and honest manner.
 Allow the client to participate in own care depending on ability and degree of
paralysis; allow to make informed choices about ADL as soon as possible.
 Teach about disease condition and manifestation.
 Discuss each procedure or type of therapy, effects of any diagnostic tests to client
and family members.
 Teach family members and client that degree of severity varies but
motor weakness and paralysis start with extremities and move upward with the
peak reached in 3 weeks and improvement seen by 4 to 8 weeks.

PROGNOSIS:
  The length of time and the amount of effort required to bring about the best possible
recovery varies among individuals and is related primarily to the severity of the
symptoms.
 About 30% of persons affected with GBS have some degree of residual weakness
after three years.
 3 - 5% may suffer a relapse many years later.
 1- 5% of cases are fatal, usually due to respiratory or cardiac complications.
 Most people, however, are able to recover completely and lead normal lives.

JOURNAL ABSTRACT:
A study was conducted on Guillain-Barré syndrome: a prospective, population-based
incidence and outcome survey by Chio A, Cocito D, Leone M, Giordana MT, Mora G,
Mutani R, et al.

Objective of this study was the incidence and long-term prognostic factors of Guillain-Barré
syndrome (GBS) in a prospective, population-based study. Study was conducted among
Patients with GBS diagnosed according to National Institute of Neurological and
Communicative Disorders and Stroke criteria in the 2-year period 1995 to 1996 in two Italian
regions were prospectively followed up for 2 years after onset of GBS. A total of 120 patients
were found, corresponding to a crude annual incidence rate of 1.36/100,000. A total of 7
(5.8%) patients, all but one with axonal pattern, died acutely within 30 days from the onset of
the disease. Acute mortality was due to respiratory involvement and intensive care unit
complications. In multivariate analysis, a worse 2-year outcome was related to a higher grade
and absence of respiratory infections preceding GBS. The persistence of disability 2 years
after the acute phase was related to axonal involvement.

After adjustment to US population, the incidence rates for GBS from different countries
showed no significant differences. Both acute mortality and long-term disability in GBS seem
to be related to an axonal involvement.

CONCLUSION:
GBS typically causes acute, rapid, and progressive ascending motor weakness. Early
recognition and treatment are crucial, especially for patients who need mechanical
ventilation. The two therapeutic options for GBS that have been shown to be the most
effective in improving symptoms. The syndrome has a 3% to 5% mortality.

BIBLIOGRAPHY:
  Brunner and Suddarth’s . “A Text book of Medical Surgical Nursing”. Vol-2. 13 th
edition, New Delhi , Wolters Kluwer; 2014, page no. 1958-1961.
 Lewis’s “Medical Surgical Nursing”, 7th edition. Published by Elsevier. Page no.
1397-1398.
 Myoclinic .Guillain-Barre syndrome[update on Jan. 15, 2020 ] available from
https://www.mayoclinic.org/diseases-conditions/guillain-barre-syndrome/diagnosis-
treatment/drc-20363006
  Chio A, Cocito D, Leone M, Giordana MT, Mora G, Mutani R, et al. Guillain-Barre
syndrome: A prospective, population-based incidence and outcome
survey. Neurology. 2003;60:1146–50. 

REFFERENCES:
 Guillain-Barre syndrome : Available from https://www.slideshare.net/drmo3/guillain-
barre-syndrome-gbs
 Guillain- Barre syndrome: Available from
https://www.slideshare.net/PraveenNagula/guillain-barre-syndrome-9053782