GBS presented by imran khan, student of BSc nursing Khyber Medical University Peshawar Pakistan.

1. 1/4/2016
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GUILLAIN-BARRE
SYNDROMESYNDROME
GUILLAIN-BARRE
SYNDROMESYNDROME
Imran Khan Salarzai
IMRANKHANSALARZAI

2. OBJECTIVES
at the end of this presentation the student will
be able to:
Define GBS.
Identify the prevelance of GBS.
Discus the causes of GBS.
Describe the pathophysiology of GBS.
Identify S/S of GBS.
Explain the diagnosis of GBS.
Discus medical management of GBS.
Formulate Nursing diagnosis and intervention of
GBS.
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3. GUILLAIN-BARRE SYNDROME
 GUILLAIN-BARRE SYNDROME (GBS) is
an acute inflammatory process that
involves degeneration of the myelin
sheath of peripheral nerves characterized
by varying degrees of motor weakness and
paralysis.
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4. PREVALENCE
 1.9 per 100, 000 persons are affected
 85% have complete recovery within 6-12
months.
 7-15% experience permanent damage
including persistent weakness, sensory
loss.
 Mortality rates vary but < 5%.
 Occurs at all ages, peak in young
adulthood (15-35yrs) and elderly person
(50-70yrs).
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5. CAUSES:
 Idiopathic.
 post infections.
 RT and GIT infection.
 campylobacter jejuni . (20 to 30%)
 EBV and CMV. (13%)
 mycoplasma pneumonia.
 Recent immunization.
 MMR vaccine.
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6. PATHOPHYSIOLOGY
 GBS is a post infectious, immune-mediated
disease. Cellular and humoral immune
mechanisms probably play a role in its
development. Most patients report an
infectious illness in the weeks prior to the
onset of GBS. Many of the identified infectious
agents are thought to induce production of
antibodies that cross-react with specific
gangliosides and glycolipids, such as GM1 and
GD1b, that are distributed throughout the
myelin in the peripheral nervous system.
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7. CONT….
 The pathophysiologic mechanism of GBS
can be typified by Campylobacter jejuni
infections. The virulence of C jejuni is
thought to be based on the presence of
specific antigens in its capsule that are
shared with nerves.
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8. CONT…
 Immune responses directed against
lipopolysaccharide antigens in the capsule of C
jejuni result in antibodies that cross-react with
ganglioside GM1 in myelin, resulting in
immunologic damage to the peripheral nervous
system. This process has been termed molecular
mimicry.
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9. CONT…
 Pathologic findings in GBS include lymphocytic
infiltration of spinal roots and peripheral nerves
(cranial nerves may be involved as well), followed
by macrophage-mediated, multifocal stripping of
myelin. This phenomenon results in defects in
the propagation of electrical nerve impulses, with
eventual absence or profound delay in
conduction, causing flaccid paralysis. Recovery is
typically associated with remyelination.
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11. SIGN & SYMPTOMS
 Motor Manifestations:
 Ascending symmetric muscle weakness flaccid paralysis
without muscle atrophy
 Decreased or absent deep tendon reflexes (DTRs)
 Respiratory compromise (dyspnea, diminished breath
sounds, decreased tidal volume and vital capacity) and
respiratory failure
 Loss of bowel and bladder control (less common)
 Sensory Manifestation:
 Paresthesias & Pain (cramping)
 Numbness generally begin in the toes and fingertips.
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12. CONT….
• Cranial Nerve Manifestations:
– Facial weakness
– Dysphagia
– Diplopia
– Difficulty speaking
• Autonomic Manifestations
– Labile blood pressure
– Cardiac dysrhythmias
– Tachycardia.
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13. DIAGNOSIS
 Hx:
 Loss of reflexes such as the knee jerk reaction can be an early
clue to a clinician.
 Lumber puncture.
 Elevated protein level in CSF
 Nerve conduction ( slow)
 Electromyography (EMG)
 Altered Respiratory function
 MRI
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15. MANAGEMENT
 IV Immunoglobulin (IVIG)
 Act by reducing the amount of anti-myelin antibodies
through the binding of the defective antibodies by
healthy antibodies contained in the IVIG solution,
and in suppressing the immune response.
 Plasmapheresis
 Symptomatic management
 Prevent complications
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16. NURSING DIAGNOSIS
• Inability to sustained spontaneous ventilation
related to progression of disease process.
• Risk for aspiration related to dysphagia.
• Pain related to paraesthesias.
• Impaired verbal communication related to
intubation or paralysis of muscles of speech.
• Self-care deficit related to inability to use
muscles to accomplish ADL.
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17. NURSING INTERVENTIONS
 Assess pain.
 Administer analgesics (NSAIDS to opioids).
 Cardiac monitoring (tachycardia).
 Elevate bed to 30o at night to reduce
orthostatic hypotension.
 Treat severe hypertension with short acting
antihypertensive drugs.
 encourage patient and his or her family.
 Establish sleep routine, administer sedatives
and hypnotics if needed.
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18. CONT….
Use devices to reduce risk of skin break down.
Assess frequently for wounds and skin break
down.
Assess gag, cough and swallow reflex to prevent
choking and monitor pharyngeal function.
Patent airway.
Oxygen administration.
Suctioning, adjusting the endotracheal or
nasotracheal airways.
Chest physiotherapy.
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