Acute onset infection Monophasic immune mediated polyneuropathy Rapid progressive motor paralysis Affects people of all ages and is not hereditary Post infectious disease It can follow by systemic infections Auto immune in nature OTHER TERMS Acute inflammatory demyelinating poly radiculopathy (AIDP) Acute idiopathic poly radiculo neuritis Acute idiopathic neuritis French polio Landry Guillain Barre Syndrome TYPES - Acute inflammatory demyelinating poly radiculo neuropathy (AIDP) Acute Motor Axonal neuropathy(AMDN) Acute Motor &Sensory Axonal neuropathy(AMSAN) Miller Fisher Syndrome(MFS) Polyneuritis Cranialis CLINICAL MANIFESTATIONS Paresthesia is frequent followed by paralysis in the extremities Hypotonia Areflexia Autonomic dysfunctions include orthostatic hypotension Hypertension Abnormal vagal responses Bowel and bladder dysfunction Facial flushing Diaphoresis Syndrome of inappropriate anti diuretic hormoneProgression of Guillain barre syndrome include lower brain stem that involves the Facial Nerve Abducens Nerve Oculo Motor Nerve Hypoglossal Nerve Trigeminal Nerve Vagus Nerve Pain Is a common symptom and It becomes worse at Night. TREATMENT On set to two weeks: Plasma pheresis (40-50 ml/kg four times a week After two weeks: intravenous administration of high dose immunoglobulin (Sandoglobulin) Beyond three weeks: plasma exchange and immunoglobulin therapies Chest Physiotherapy Artificial ventilation-Maintain Gas Exchange COMPLICATIONS Cardiac arrhythmias Respiratory failures Dys autonomia Pneumonia Adult Respiratory Distress Syndrome Septicemia Death

1. Mrs. A.Sarmila
Associate Professor
GUILLAIN BARRE SYNDROME(GBS)

2. INTRODUCTION
 Acute onset infection
 Monophasic immune mediated polyneuropathy
 Rapid progressive motor paralysis
 Affects people of all ages and is not hereditary
 Post infectious disease
 It can follow by systemic infections
 Auto immune in nature

3. NEURON

4. DEFINITION
• It is a rapidly progressing
and potentially fatal form
of polyneuritis.
• It affects the peripheral
nervous system and
results in loss of myelin
and edema and
Inflammation of affected
nerves causing a loss of
neuro transmission to the
periphery.

5. OTHER TERMS
 Acute inflammatory demyelinating poly
radiculopathy (AIDP)
 Acute idiopathic poly radiculo neuritis
 Acute idiopathic neuritis
 French polio
 Landry Guillain Barre Syndrome

6. INCIDENCE
 The annual incidence of GBS ranges from
0.5-1.5 cases from 1,00,000 population.
 Mostly affected group are individuals less than
18 yrs.
 Males are appear to be great risk than females.

7. CAUSES
• Unknown
 Auto immune disease triggered by
 Bacterial- Campylobacter jejuni, Mycoplasma
pneumoniae
 Virus- Ebstein barr virus, Cytomegalo virus
 Skipping vaccination against Flu, Rabies,
Meningitis

8. PHASES
Progressive phase:
worsening symptoms-4weeks
73% reach lowest point of clinical function at 1 week
98% at 4 weeks,30% ventilatory assistance
20% mortality rate.
Plateau phase: persistent unchanging
symptoms days

9. CONT…
Recovery: Improvement in symptoms &
functioning
• 85% full and functional recovery with in 6-12
months
• Maximal by 18 months past onset
• Relapse occurs in 3-5% patients

10. TYPES
 Acute inflammatory demyelinating poly radiculo
neuropathy (AIDP)
 Acute Motor Axonal neuropathy(AMDN)
 Acute Motor &Sensory Axonal
neuropathy(AMSAN)
 Miller Fisher Syndrome(MFS)
 Polyneuritis Cranialis

11. ACUTE INFLAMMATORY DEMYELINATING
POLY RADICULO NEUROPATHY (AIDP)
 80-90%cases of GBS are in this type.
 Immune mediated attack of myelin with infiltration of
lymphocytes and macrophages with segmental
stripping of myelin. Motor and sensory fibres are
affected.

12. ACUTE MOTOR AXONAL
NEUROPATHY(AMDN)
 Axonal degeneration occurs after an immune
attack with in 1-2 weeks after infection.
 Specific antibodies to axonal membranes of
motor fibres attack the nodes of Ranvier.
This in turns activates compliment system and
intrusion of macrophages in to periaxonal spaces
to cause axon destruction.

13. ACUTE MOTOR AND SENSORY AXONAL
NEUROPATHY(AMSDN)
 This type is rare resembles AMAN except
sensory nerves are also affected.
 This type is associated with a severe course and
poor prognosis.
.

14. MILLER FISHER SYNDROME (MFS)
 This involvement of CN’s is very distinct in the
form of GBS.
Oculomotor nerves (Oculo motor, Trochlear and
abducens)are affected and produce a triad of
Ophthalmoplegia, Ataxia. Areflexia.

15. POLY NEURITIS CRANIALIS
This is an acute onset of multiple Cranial nerve
palsies.
Usually Bilateral Cranial nerve VII With sparing
of Cranial nerves 1,2.
Elevated CSF protein
Slowed nerve conduction velocity

16. PATHOPHYSIOLOGY
Organisms /Trauma
Cell mediated and hormonal immune reaction in the
peripheral nerve myelin protein
Migration of macrophages and other immune
mediated agent at the site of inflammation
Destruction of myelin layer (demyelination) and edema
Interruption of nerve conduction
Weakness with dyskinesia, hyporeflexia, and paresthesia

17. CLINICAL MANIFESTATIONS
 1-3 weeks after an upper respiratory or gastro
intestinal infection.
 There will be weakness of the lower extremities
(evolving more or less symmetrical)
 It occurs over hours to days to weeks
 It usually peaks on the 14th day

18. CONT….
• Paresthesia is frequent followed by paralysis
in the extremities
• Hypotonia
• Areflexia
• Objective sensory loses variable with deep
sensitivity in superficial sensations

19. CONT….
• Autonomic dysfunctions include orthostatic
hypotension
• Hypertension
• Abnormal vagal responses
• Bowel and bladder dysfunction
• Facial flushing
• Diaphoresis
• Syndrome of inappropriate anti diuretic hormone

20. CONT..
Progression of Guillain barre syndrome
include lower brain stem that involves the
 Facial Nerve
 Abducens Nerve
 Oculo Motor Nerve
• Hypoglossal Nerve
• Trigeminal Nerve
• Vagus Nerve
• Pain Is a common symptom and It becomes worse
at Night.

21. DIAGNOSTIC EVALUATION
 History collection
 Neurological examination
• First 48hrs -Cerebro spinal
fluid is normal, after that it
shows a low protein content.
• After 7-10 days it is elevated to
700mg/dl (normal 15-45 mg/dl).

22. CONT…
 CSF: Normally Fewer 10 leukocytes but occasionally
elevated .
 Electromyography
 Nerve conduction studies
 Lumbosacral MRI
 Serum Anti Ganglioside Antibodies

23. COMPLICATIONS
 Cardiac arrhythmias
 Respiratory failures
 Dys autonomia
 Pneumonia
 Adult Respiratory Distress Syndrome
 Septicemia
• Death

24. TREATMENT
• On set to two weeks: Plasma pheresis (40-50 ml/kg
four times a week
• After two weeks: intravenous administration of high
dose immunoglobulin (Sandoglobulin)
• Beyond three weeks: plasma exchange and
immunoglobulin therapies
• Chest Physiotherapy
• Artificial ventilation-Maintain Gas Exchange

25. NURSING DIAGNOSIS
• Impaired spontaneous ventilation related to
progression of disease process resulting in respiratory
muscle paralysis
• Acute pain related to paresthesias, muscle aches,
cramps and hyperesthesia
• Impaired verbal communication related to intubation or
paralysis of muscles of speech
• Self care deficit related to inability to use muscles to
accomplish activities of daily living

26. NURSING MANAGEMENT
• assess the ascending paralysis, respiratory function,
arterial blood gases, gag, corneal and swallowing
reflexes ,monitor blood pressure and heart rate
• perform bronchial hygiene and chest physiotherapy
• perform intermittent catheterization
• perform range of motion exercise
• provide artificial tears and moisturizers
• provide intravenous fluids

27. REFERENCES
Books:
• Hasper, Fauci, Hauzer et.al, (2015)“Harrison’s Principles of
Internal Medicine” Published by Mc Grew hills companies,
19th Edition.
• Brunner& Suddarth’s(2013),Textbook of Medical-Surgical
Nursing”. Published by Lippincott Williams & Wilkins, 6th
Edition.
Web sources:
• http://brain foundation.org.au/disorders/guillain barre syndrome
• www.betterhealth.vic.gov.au/health/conditionsandtreatment
/guillain barre syndrome.