Guillain Barre Syndrome

(GB Syndrome)
• Guillain-Barre Syndrome(GBS) is an acquired inflammatory
disease that results in demyelination of the peripheral nerves
with relative sparing of axons.
• The patient has a progressive ascending paralysis that is usually
reversible
Sub-types/Variants of GBS
 Acute Inflammatory Demyelinating
Polyneuropathy(AIDP)

 The most common form

 Prevalent in western countries
 Adults are affected more than the children
 Attacks the Schwann cell and axons remains intact
 Recovery is rapid as remyelination occurs
 Primary Acute Motor Axonal Neuropathy (AMAN)

 Prevalent in China & Mexico

 Children and young subjects are affected more than adults

 Directed against the axon & Nodes of Ranvier

 Recovery takes place when axon regeneration is complete and

it is rapid when lesion is localized
 Acute Motor-Sensory Axonal Neuropathy(AMSAN)

 Very rare

 Closely related to AMAN

 Adults are mostly affected

 Axonal damage is severe

 Recovery is slow and often incomplete

 Miller-Fisher Syndrome
 Adults ,young subjects and children are affected

 Involves PNS & CNS structures

 Pathological features resemble that of AIDP

 Characterized by rapidly evolving of Triad;

- Ataxia ( mostly in gait and trunk)

- Opthalmoplegia

- Areflexia
 Recovery can be rapid
Causes
•Respiratory infection

•Gastrointestinal infection

• Vaccination (rabies, tetanus, influenza)

• Pregnancy

•Surgery

•Infection with campylobacter jejuni

 Pathophysiology
An infectious organism contains an amino acid that mimics the
peripheral nerve myelin protein

The immune system cannot distinguish between the two proteins

Infectious organism attack the ganglioside ( location in PNS)

 Pathophysiology
Influx of macrophages and other immune mediated agents

Inflammation and destruction

Axon unable to support nerve conduction

 Clinical Manifestations
• Classic clinical features include areflexia and ascending weakness

• Muscle weakness and diminished reflexes of the lower extremities

• Hyporeflexia and weakness ----- quadriplegia

• Involvement of diaphragm and intercostal muscles ---

neuromuscular respiratory failure
• Sensory symptoms include

• Paresthesias of the hands and feet

• Pain
 Clinical Manifestations
• Optic nerve --- blindness

• Glossopharyngeal --- bulbar muscle weakness

• Vagus nerve --- swallow or clear secretions,

• Vagus nerve demyelination results in cardiovascular system

instability (tachycardia, bradycardia, hypertension,
orthostatic hypotension)
• Does not affect cognitive function or level of consciousness
 Assessment and Diagnostic Findings
• The patient presents with symmetric weakness, diminished
reflexes and upward progression of motor weakness
• A history of a viral illness in the previous few weeks suggests
the diagnosis
• Changes in vital capacity and negative inspiratory force

• CSF: only elevated protein levels

• Evoked potential studies: progressive loss of nerve conduction

velocity
Management
 Medical management

a) IVIg(Intravenous Immunoglobulin)

a) Plasmapheresis
 Medical Management
• Plasmapheresis and IVIG are used to directly affect the
peripheral nerve myelin antibody level.
• Both therapies decrease circulating antibody levels and
reduce the amount of time the patient is immobilized and
dependent on mechanical ventilation.
• Studies indicate that IVIG and plasmapheresis are equally
effective in treating GBS
 Medical Management
• Medical emergency

• ICU management

• Assessment of respiratory function- respiratory therapy and

mechanical ventilation
• Prevention of complications of immobility- anticoagulant
agents and thigh high elastic compression stockings
 Medical Management
• Continuous ECG monitoring

• Tachycardia and hypertension -- short-acting medications

such as alpha-adrenergic blocking agents
• Hypotension --- is managed by increasing the amount of IV
fluids
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Physiotherapy Management
 Nursing management
• Ineffective airway clearance related to rapidly progressive
weakness and impending respiratory failure

• Impaired physical mobility related to paralysis

• Imbalanced nutrition: less than body requirements related to

inability to swallow

• Impaired verbal communication related to cranial nerve

dysfunction
•Anxiety related to loss of control and paralysis
 Interventions
• Maintaining respiratory function
- Incentive spirometry and chest physiotherapy

- Monitor changes in vital capacity

- Mechanical ventilation

- Suctioning

- Assess the blood pressure and heart rate frequently

- Medications / temporary pacemaker for clinically significant

bradycardia
 Interventions
• Enhance physical mobility

• Support the paralyzed extremities in functional position

• Passive range-of-motion exercises

• Prevention of DVT

• Prevention of pressure ulcer

• Meet nutrition and hydration needs

 Interventions
• Provide adequate nutrition

• administer IV fluids and parenteral nutrition

• monitor for the return of bowel sounds

• gastrostomy tube placement

• Assess for gag reflex and bowel sounds

 Interventions
• Improve communication

• Establish some form of communication with picture cards or an

eye blink system
• Collaboration with the speech therapist

• Decreasing fear and anxiety

• Referral to a support group

• Involve family members in care

• Provide information about the condition

• Teaching relaxation exercises and distraction techniques

 Interventions
• Monitoring and managing potential complications

• Thorough assessment of respiratory function

• Vital capacity is monitored frequently

• Monitor for complications and pay attention to prevent them

and be prompt
Thank You