lOMoARcPSD|11404906
Guillain Barre Syndrome
What is it?
 Autoimmune attack of the peripheral
nerve myelin
Result: acute, rapid segmental demyelination
of peripheral and cranial nerves.
- Ascending weakness
- Dyskinesia (impaired ability to execute
voluntary movement)
- Hyporeflexia
- Paresthesias
An infection usually precedes the
development
Epstein-Barr, HIV, Campylobacter jejuni,
cytomegalovirus, mycoplasma pneumoniae, H.
influenza

Pathophysiology:
 Myelin – Covers the nerve providing insulation
and speed for conduction from the cell body
to the dendrite
 Schwann cells produce myelin (which is not
destroyed in the disease and allows for remyelination)
 GBS- results in cell mediated and humoral
immune attack of the myelin proteins
Causing inflammation and demyelination
Theory: the infectious organism contains a
protein that mimics that of the myelin protein in
the periphery
Therefore, since the body cannot distinguish
between the two proteins, it attacks both. The
immune system attack causes macrophages and
other immune mediated agents to influx into the
area
Inflammation, myelin destruction, interruption of
nerve conduction, axonal loss
Clinical Manifestations:
 Usually antecedent is 2 weeks before disease
begins
 Weakness and hyporeflexia will begin in the
legs and spread to the arms
 Weakness and paralysis in the intercostal
muscles and the diaphragm can lead to
respiratory failure
-Mechanical ventilator
Sensory symptoms:
 Parasthesias
 Pain- due to demyelination of the sensory
fibers
May affect the cranial nerves
 Vagus- autonomic dysfunction, instability of
cardiac system (Tachycardia, bradycardia,
hypertension, hypotension)
 Optic nerve- blindness
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 Glossyopharyngeal and Vagus nerve – inability
to swallow and clear secretions (Bulbular
muscle weakness)
Medical Management:
 Patient will be in the ICU setting due to
rapid progression
 Elective intubation is recommended
 Patient is weaned of ventilator when
they are having spontaneous
respirations and can maintain
adequate O2
 Prevent immobility complications
 Plasmapheresis and IVIG
Decrease the circulating antibodies,
improves recovery time
IVIG – fewer S/E
 When treating autonomic dysfunctionmake sure to use short term solutions
Nursing Diagnoses:
 Ineffective breathing pattern and
impaired gas exchange R/T rapidly
progressing weakness and impending
respiratory failure
 Impaired physical mobility related to
paralysis
 Imbalanced nutrition, less than body
requirements, R/T inability to swallow
 Impaired verbal communication R/T
cranial nerve dysfunction
 Fear and anxiety R/T loss of control
and paralysis
Does not affect cognitive or LOC
Recovery may take up to 2 years some of the
changes may be permanent
Assessment:
 Look for a recent viral illness, with a sudden
changes including:
-Symmetric weakness
-Diminished reflexes
-Upward progression of weakness
 The progression of the disease is sudden
 Watch for progression and complication
 Complications:
DVT, PE, respiratory failure, cardiac
dysrhythmias, autonomic
dysfunction
Goals and Interventions:
Improve respiratory function
 Monitor for changes in vital capacity and
negative inspiratory forces- If they fall,
patient will need a ventilator
 Discuss ventilator on admission – decrease
anxiety
 Inability to swallow and clear secretions may
also cause respiratory failure- frequent
suctioning needed
 Autonomic dysfunction is assessed and
treated as needed
Increase mobility
 Must enhance mobility and prevent
complications of immobility
Improve nutritional status
 Gastrostomy tubes may be placed if the
patient cannot swallow
 Patient may develop a paralytic ileus – due to
lack of parasympathetic activity ……
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parenteral nutrition may become necessary
 Monitor for bowel sounds and gag reflex
Effective communication
 The patient will not be able to talk, laugh, or
cry due to paralysis
 Establish a system of communication (Blinking
eyes, cards)
Decrease fear and anxiety
 Sudden, life threatening disease
 Allow the family to participate in daily care
 Patient may fell isolation, loneliness, and fear
Absence of complications
 Assess respiratory function frequently
because changes may be sudden
 Respiratory rate, quality, vital capacity
 S/S of impending respiratory failure:
breathless while speaking, shallow an
irregular breathing, use of accessory
muscles, tachycardia, weak cough, changes
in respiratory pattern
 Autonomic dysreflexia
 Treat changes with short acting solutions
Teaching: most patients make a complete recovery
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