Guillain-Barré syndrome is an autoimmune disorder where the immune system attacks the peripheral nervous system, causing demyelination of nerves. It is usually preceded by a bacterial or viral infection. Clinical features include ascending weakness, diminished reflexes, and sensory symptoms like numbness. Treatment involves plasmapheresis or IVIG to modulate the immune response, as well as supportive care like ventilation if needed. Nurses monitor for respiratory failure and other complications and focus on maintaining mobility, nutrition, communication, and managing fear and anxiety.

1. Mr. HIREN GEHLOTH
JG COLLEGE OF NURSING

2. • Guillain-Barré syndrome is an autoimmune attack on the peripheral nerve
myelin. The result is acute, rapid segmental demyelination of peripheral
nerves and some cranial nerves, producing ascending weakness with
dyskinesia (inability to execute voluntary movements), hyporeflexia, and
paresthesia's (numbness).
GUILLAIN BARRE SYNDROME

4. DEFINITION:
“GBS is a acute
demyelinating disorder of the
peripheral nervous system that
result from an aberrant immune
response at peripheral nerves.”
GUILLAIN BARRE SYNDROME

6. ETIOLOGY AND RISK
FACTORS
• Campylobacter jejuni,
• cytomegalovirus,
• Epstein-Barr virus,
• Mycoplasma pneumoniae,
• H. influenzae,
• and HIV are the most common infectious agents that
are associated with the development of Guillain-Barré
syndrome.
Exact Cause is Unknown

7. RISK FACTORS

8. PATHOPHYSIOLOGY
Myelin is a complex substance that covers
nerves, providing insulation and speeding the
conduction of impulses from the cell body to
the dendrites. The cell that produces myelin in
the peripheral nervous system is the Schwann
cell. In Guillain-Barré syndrome, the Schwann
cell is spared, allowing for remyelination in the
recovery phase of the disease.
IF DAMAGE HAS OCCURRED TO AXONS, THEN REGROWTH IS
REQUIRED AND TAKE MONTHS OR YEARS AND IS OFTEN
INCOMPLETE.

9. Cell Mediated
Immunity Humoral Immunity
The infectious agents contains the amino acid that
mimic with the peripheral nerve myelin protein.
The Immune system or lymphatic can’t differentiate
between the two proteins.
Attacks and destroy the peripheral nerve myelin.
Defects in the transmission of the nerve impulses and
eventually conduction block
Dyskinesia Hyporeflexia Paresthesia's
THE MOLECULAR MIMICRY MECHANISM

15. CLINICAL FEATURES
Classic clinical features of GBS include areflexia and
weakness, although there may be variations in
presentation.
Initial symptoms include :
• muscle weakness
• diminished reflexes of the lower extremities;
(hyporeflexia)
• weakness may progress to tetraplegia;
• demyelination of the nerves that innervate the
diaphragm and intercostal muscles results in
neuromuscular respiratory failure.
REMEMBER THIS,
GBS DOES NOT AFFECT COGNITIVE FUNCTION OR LOC.

16. • Sensory symptoms include paresthesia's of the hands and feet
and pain related to the demyelination of sensory fibers.
• Optic nerve demyelination may result in blindness.
• Bulbar muscle weakness related to demyelination of the
glossopharyngeal and vagus nerves results in the inability to
swallow or clear secretions.
• Vagus nerve demyelination results in autonomic dysfunction,
manifested by instability of the cardiovascular system
(tachycardia, bradycardia, hypertension, or orthostatic
hypotension).

17. • Clinical presentation (symmetric weakness, diminished
reflexes, and upward progression of motor weakness) and
history of recent viral infection.
• Changes in vital capacity and negative inspiratory force
are assessed to identify impending neuromuscular
respiratory failure.
• Elevated protein levels are detected in cerebrospinal
fluid (CSF) evaluation, without an increase in other cells.
• Evoked potential studies demonstrate a progressive loss
of nerve conduction velocity.
ASSESSMENT AND DIAGNOSTIC
FINDINGS

18. • GBS is considered a medical emergency; patient is
managed in an intensive care unit.
• Respiratory problems may require respiratory therapy or
mechanical ventilation.
• Elective intubation may be implemented before the
onset of extreme respiratory muscle fatigue.
• Anticoagulant agents and antiembolism stockings or
sequential compression boots may be used to prevent
thrombosis and pulmonary emboli.
MEDICAL MANAGEMENT

19. • Plasmapheresis (plasma exchange)
> During plasmapheresis, blood is
removed from body and passes
through a machine that separates
blood cells. The separated cells are
then returned to body with new
plasma. This procedure may help
shorten the course and sensitivity of
Guillain Barre Syndrome.

20. • Intravenous immunoglobulin (IVIG) may be used to directly affect the
peripheral nerve myelin antibody level.
• Continuous ECG monitoring: Observe and treat cardiac dysrhythmias and
other labile complications of autonomic dysfunction. Tachycardia and
hypertension are treated with short-acting medications such as alpha-
adrenergic blocking agents. Hypotension is managed by increasing the
amount of intravenous fluid administered.

21. NURSING
MANAGEMENT
Assessment
• Monitor the patient for life-threatening complications (respiratory failure,
cardiac dysrhythmias, deep vein thrombosis [DVT]) so that appropriate
interventions can be initiated.
• Assess the patient’s and family’s ability to cope and their use of coping
strategies.

22. Nursing Diagnoses
• Ineffective breathing pattern and impaired gas exchange related to rapidly
progressive weakness and impending respiratory failure
• Impaired bed and physical mobility related to paralysis
• Imbalanced nutrition, less than body requirements, related to inability to swallow
• Impaired verbal communication related to cranial nerve dysfunction
• Fear and anxiety related to loss of control and paralysis

23. Nursing Interventions
• Maintaining Respiratory Function
• Enhancing Physical Mobility
• Providing Adequate Nutrition
• Improving Communication
• Decreasing Fear and Anxiety
• Monitoring and Managing Potential Complications
• Assess respiratory function at regular and frequent intervals; monitor respiratory
rate, the quality of respirations, and vital capacity.
• Watch for breathlessness while talking, shallow and irregular breathing, use of
accessory muscles, tachycardia, weak cough, and changes in respiratory pattern.
• Monitor for and report cardiac dysrhythmias (through ECG monitoring), transient
hypertension, orthostatic hypotension, DVT, pulmonary embolism, and urinary
retention.