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GUILLAIN Barrie
Syndrome
Presented By: Rubina Shehzadi BSN, Mphil Public Health
Presentation Outline
At the end of this presentation, you will be able to learn:
Definition OF GBS
Epidemiology
Etiology
Pathogenesis
Risk factors &Clinical features
Investigations
Diagnosis
Treatment
Nursing Management
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".
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.
Introduction
“It is an acquired ,frequently severe ,monophasic
autoimmune illness of Peripheral Nervous
System(PNS)”
Guillain-Barre syndrome
• 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.
• It involves mostly motor but also sensory and autonomic nerves.
• “Guillain-Barré Syndrome (GBS) is an acute demyelinating disorder of
the peripheral nervous system that results from an aberrant immune
response directed at peripheral nerves”
Guillain-Barre syndrome
• Guillain-Barre syndrome (GBS) is a rare neurological disorder in which
the body's immune system mistakenly attacks part of its peripheral
nervous system.
• After the advent of OPV ,today GBS is almost the only inflammatory
Polyneuropathy and most frequent cause of acute flaccid paralysis
in general medical practice.
Alternative names
• It is also known as:
• Guillain-Barre-Strohl Syndrome (First described in 1916 by French Physician)
• Post-Infectious Polyneuropathy
• Acute Idiopathic Polyneuropathy
• Landry’s Paralysis
Epidemiology
• In recent study (2018), frequency is 1.1-1.8 per100,00 population in
Pakistan. (Sindh& KPK)
• Throughout the world with a medium incidence of 1.3 /100,000
population
• Males are more commonly affected than females
• Peaks in young adults and in elderly
• Approximately 85% patients recover spontaneously while 10%
patients need hospitalization
• Its prevalence has been reported to vary from region to region
Types of GBS
GBS
AIDP
AMAN
AMSAN
MFS
Types of GBS
1. Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
2. Miller-Fisher Syndrome (MFS)
3. Acute Motor-Sensory Axonal Neuropathy(AMSAN)
4. Acute Motor Axonal Neuropathy (AMAN)
Etiology
1. Unknown
2. GIT infection
1. Campylobacter jejuni (26-41%)
2. Cytomegalovirus (10-22%)
3. Respiratory tract infection
1. Mycoplasma pneumoniae
4. Ebstein-Barr virus (10%)
5. Vaccines
• – Rabies
• – Avian-flu influenza
Risk Factors & Clinical Features
Clinical Features
• Parathesias
• Ascending paralysis
• Poorly localized pain. Pain (90% of patients) described like a “Charlie
horse.”
• Absent reflexes
• Breathing difficulties
• Gait abnormality due to muscle weakness
• Facial nerve abnormalities
• Autonomic instability (cardiac dysrhythmias, orthostatic hypotension,
hypertension, paralytic ileus, transient bladder dysfunction)
Pathogenesis
• GBS occurs in relatively healthy persons that experience an
antecedent infection/event anywhere from days to weeks prior to
onset of GBS symptoms.
• Autonomic abnormalities in GBS are usually transient and reversible.
Conti…
Diagnosis Criteria
Requires that the following criteria are met: (AIDP)
1. Areflexia
2. Include in differential and rule out other causes
3. Duration < 4 weeks
4. Progressive weakness of 2 or more limbs due to neuropathy
5. Protein Elevation in CSF
2.
4
Course
Initial phase
• – Gradually increasing involvement lasts 10-30 days
• (less than 4 weeks)
Plateau phase
• – Short phase (within 2 weeks)
• – Long plateau phase → poor prognosis
Recovery phase
• – Within months
• – Usually complete
• – Motor sequelae (5-25%)
• – Relapse & late recurrences (3%)
Investigations
• CSF: Elevated protein without an elevated cell count
• EMG: Later in disease, It shows signs of
demyelination.
• Serum Creatine Kinase: Elevated or normal
• NCS
• PFTs
• Muscle biopsy: show evidence of denervation atrophy in
• 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.
Conti…
• Patients with rapidly progressive ascending paralysis:
• Intravenous immunoglobulin (IVIG), administered for 2, 3, or 5 days
• Plasmapheresis, steroids, and/or immunosuppressive drugs are
alternatives, if IVIG is ineffective
• Combined administration of immunoglobulin and interferon is
effective in some patients.
• Supportive care, such as respiratory support, prevention of decubiti in
children with flaccid tetraplegia, and treatment of secondary bacterial
infections, is important.
Mnemonic:AIDP(for easy memorization)
• 1. Supportive:
• Analgesia: e.g. NSAIDs
• Airway: may need ventilator
• Autonomic: may need a urinary catheter
• Antithrombotic: TED stockings, LMWH
2. IVIG 0.4 g/kg/day for 5 days
3. Dexamethasone (corticosteroid): No significant role
4. Plasma exchange (Plasmapheresis): Alternative to IVIG; 5 times
during 2 weeks
3 clinical features predictive to poor outcome:
1. – Cranial nerve involvement
2. – Intubation
3. – Maximum disability at the time of presentation
Nursing Diagnoses
1. Ineffective Breathing Pattern r/t ascending paralysis as
evidenced by respiratory changes, abnormal ABGs, cyanosis.
2. Acute Pain r/t inflammation of nerves as evidenced by pain scale,
tachypnea, tachycardia, diaphoresis.
3. Impaired Physical Mobility r/t Neuromuscular impairment as evidenced
by paralysis, decreased muscle strength.
4. Impaired Urinary Elimination r/t Neuromuscular impairment as
evidenced by urinary retention/paralysis
5. Anxiety r/t Change in health status and threat to self-concept as
evidenced by expression of helplessness or increased apprehension.
6. Risk for Impaired Skin Integrity r/t paralysis as evidenced by redness in
pressure areas
Nursing Interventions
• Assess frequency, symmetry, and depth of breathing.
• Observed for increased work of breathing and evaluate skin color,
temperature, capillary refill, Assess ABGs
• Observe for signs of respiratory fatigue such as shortness of breath,
decreased attention span, and impaired cough.
• Keep the head of bed elevated at around 35-45°.
• Perform chest physiotherapy (postural drainage, chest percussion,
chest vibration, turning, deep breathing and coughing exercises)
• Anticipate need for ventilator.
Conti…
• Administer analgesics based on pain.
• Provide support to extremities and maintain clean, comfortable
bed using egg-crate mattress and padding to bony prominences as needed
• Reposition client every 2 hours, use good postural alignment, assist with
passive ROM.
• Monitor nutritional needs.
• Perform active, passive and isotonic range of motion exercises as
appropriate.
• Monitor intake and output every 4 to 8 hours and palpate bladder every 2
hours; assess for cloudy, foul-smelling urine.
• Reassurance of patient
Conti…
• if needed, insert an indwelling urinary catheter to maintain
elimination.
• Teach patients about disease condition and manifestation and Discuss
each procedure or type of therapy, effects of any diagnostic tests.
• Clarify any information and answer questions in lay terms and utilize
visual aids for reinforcement if helpful.
• Teach about physical therapy program including ROM, exercises, gait
training, bracing.
SUMMARIZATION
Any Query????
Quote:
“The Doors will be opened to Those who
are Bold enough to Knock”

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Gullian barrie syndrome (gbs)

  • 1.
  • 2. GUILLAIN Barrie Syndrome Presented By: Rubina Shehzadi BSN, Mphil Public Health
  • 3. Presentation Outline At the end of this presentation, you will be able to learn: Definition OF GBS Epidemiology Etiology Pathogenesis Risk factors &Clinical features Investigations Diagnosis Treatment Nursing Management
  • 4. 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".
  • 5. 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.
  • 6. Introduction “It is an acquired ,frequently severe ,monophasic autoimmune illness of Peripheral Nervous System(PNS)”
  • 7. Guillain-Barre syndrome • 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. • It involves mostly motor but also sensory and autonomic nerves. • “Guillain-Barré Syndrome (GBS) is an acute demyelinating disorder of the peripheral nervous system that results from an aberrant immune response directed at peripheral nerves”
  • 8. Guillain-Barre syndrome • Guillain-Barre syndrome (GBS) is a rare neurological disorder in which the body's immune system mistakenly attacks part of its peripheral nervous system. • After the advent of OPV ,today GBS is almost the only inflammatory Polyneuropathy and most frequent cause of acute flaccid paralysis in general medical practice.
  • 9. Alternative names • It is also known as: • Guillain-Barre-Strohl Syndrome (First described in 1916 by French Physician) • Post-Infectious Polyneuropathy • Acute Idiopathic Polyneuropathy • Landry’s Paralysis
  • 10. Epidemiology • In recent study (2018), frequency is 1.1-1.8 per100,00 population in Pakistan. (Sindh& KPK) • Throughout the world with a medium incidence of 1.3 /100,000 population • Males are more commonly affected than females • Peaks in young adults and in elderly • Approximately 85% patients recover spontaneously while 10% patients need hospitalization • Its prevalence has been reported to vary from region to region
  • 12. Types of GBS 1. Acute Inflammatory Demyelinating Polyneuropathy (AIDP) 2. Miller-Fisher Syndrome (MFS) 3. Acute Motor-Sensory Axonal Neuropathy(AMSAN) 4. Acute Motor Axonal Neuropathy (AMAN)
  • 13. Etiology 1. Unknown 2. GIT infection 1. Campylobacter jejuni (26-41%) 2. Cytomegalovirus (10-22%) 3. Respiratory tract infection 1. Mycoplasma pneumoniae 4. Ebstein-Barr virus (10%) 5. Vaccines • – Rabies • – Avian-flu influenza
  • 14. Risk Factors & Clinical Features
  • 15. Clinical Features • Parathesias • Ascending paralysis • Poorly localized pain. Pain (90% of patients) described like a “Charlie horse.” • Absent reflexes • Breathing difficulties • Gait abnormality due to muscle weakness • Facial nerve abnormalities • Autonomic instability (cardiac dysrhythmias, orthostatic hypotension, hypertension, paralytic ileus, transient bladder dysfunction)
  • 16. Pathogenesis • GBS occurs in relatively healthy persons that experience an antecedent infection/event anywhere from days to weeks prior to onset of GBS symptoms. • Autonomic abnormalities in GBS are usually transient and reversible.
  • 18.
  • 19. Diagnosis Criteria Requires that the following criteria are met: (AIDP) 1. Areflexia 2. Include in differential and rule out other causes 3. Duration < 4 weeks 4. Progressive weakness of 2 or more limbs due to neuropathy 5. Protein Elevation in CSF 2. 4
  • 20. Course Initial phase • – Gradually increasing involvement lasts 10-30 days • (less than 4 weeks) Plateau phase • – Short phase (within 2 weeks) • – Long plateau phase → poor prognosis Recovery phase • – Within months • – Usually complete • – Motor sequelae (5-25%) • – Relapse & late recurrences (3%)
  • 21. Investigations • CSF: Elevated protein without an elevated cell count • EMG: Later in disease, It shows signs of demyelination. • Serum Creatine Kinase: Elevated or normal • NCS • PFTs • Muscle biopsy: show evidence of denervation atrophy in • Nerve biopsy: segmental demyelination, focal inflammation. • Serologic testing for Campylobacter infection
  • 22. 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.
  • 23. Conti… • Patients with rapidly progressive ascending paralysis: • Intravenous immunoglobulin (IVIG), administered for 2, 3, or 5 days • Plasmapheresis, steroids, and/or immunosuppressive drugs are alternatives, if IVIG is ineffective • Combined administration of immunoglobulin and interferon is effective in some patients. • Supportive care, such as respiratory support, prevention of decubiti in children with flaccid tetraplegia, and treatment of secondary bacterial infections, is important.
  • 24. Mnemonic:AIDP(for easy memorization) • 1. Supportive: • Analgesia: e.g. NSAIDs • Airway: may need ventilator • Autonomic: may need a urinary catheter • Antithrombotic: TED stockings, LMWH 2. IVIG 0.4 g/kg/day for 5 days 3. Dexamethasone (corticosteroid): No significant role 4. Plasma exchange (Plasmapheresis): Alternative to IVIG; 5 times during 2 weeks
  • 25. 3 clinical features predictive to poor outcome: 1. – Cranial nerve involvement 2. – Intubation 3. – Maximum disability at the time of presentation
  • 26. Nursing Diagnoses 1. Ineffective Breathing Pattern r/t ascending paralysis as evidenced by respiratory changes, abnormal ABGs, cyanosis. 2. Acute Pain r/t inflammation of nerves as evidenced by pain scale, tachypnea, tachycardia, diaphoresis. 3. Impaired Physical Mobility r/t Neuromuscular impairment as evidenced by paralysis, decreased muscle strength. 4. Impaired Urinary Elimination r/t Neuromuscular impairment as evidenced by urinary retention/paralysis 5. Anxiety r/t Change in health status and threat to self-concept as evidenced by expression of helplessness or increased apprehension. 6. Risk for Impaired Skin Integrity r/t paralysis as evidenced by redness in pressure areas
  • 27. Nursing Interventions • Assess frequency, symmetry, and depth of breathing. • Observed for increased work of breathing and evaluate skin color, temperature, capillary refill, Assess ABGs • Observe for signs of respiratory fatigue such as shortness of breath, decreased attention span, and impaired cough. • Keep the head of bed elevated at around 35-45°. • Perform chest physiotherapy (postural drainage, chest percussion, chest vibration, turning, deep breathing and coughing exercises) • Anticipate need for ventilator.
  • 28. Conti… • Administer analgesics based on pain. • Provide support to extremities and maintain clean, comfortable bed using egg-crate mattress and padding to bony prominences as needed • Reposition client every 2 hours, use good postural alignment, assist with passive ROM. • Monitor nutritional needs. • Perform active, passive and isotonic range of motion exercises as appropriate. • Monitor intake and output every 4 to 8 hours and palpate bladder every 2 hours; assess for cloudy, foul-smelling urine. • Reassurance of patient
  • 29. Conti… • if needed, insert an indwelling urinary catheter to maintain elimination. • Teach patients about disease condition and manifestation and Discuss each procedure or type of therapy, effects of any diagnostic tests. • Clarify any information and answer questions in lay terms and utilize visual aids for reinforcement if helpful. • Teach about physical therapy program including ROM, exercises, gait training, bracing.
  • 32.
  • 33. Quote: “The Doors will be opened to Those who are Bold enough to Knock”