Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy that results in demyelination and inflammation of the peripheral nervous system. It presents as rapidly progressive muscle weakness that peaks within 4 weeks. GBS is usually preceded by a bacterial or viral infection. The most common type is acute inflammatory demyelinating polyneuropathy, which involves demyelination of motor and sensory fibers. Treatment involves plasma exchange or intravenous immunoglobulin to modulate the immune response. Nursing management focuses on respiratory support, pain management, range of motion exercises, and prevention of complications.

1. Prof.Kavitha.P, M.Sc (N)
Vice Principal,
Ganga College of Nursing ,
Coimbatore.

2. SUBJECT:
MEDICAL SURGICAL NURSING-II
UNIT NO:3
NURSING MANAGEMENT OF PATIENT WITH
NEUROLOGICAL DISORDERS
TOPIC:
GUILLAIN BARRE SYNDROME(GBS)

3. 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

4. OBJECTIVES
At the end of the class, the students are able to
 review anatomy and physiology of Neuron
 define Guillain Barre Syndrome
 state the incidence of Guillain Barre Syndrome
 enlist the causes and risk factors of Guillain Barre
Syndrome
 explain the types of Guillain Barre Syndrome
 narrate the pathophysiology of Guillain Barre
Syndrome.

5. CONT….
 state the clinical manifestations of Guillain Barre
Syndrome
 enlist the diagnostic measures of Guillain Barre
Syndrome
 state the complications of Guillain Barre Syndrome
 enumerate the management of patient with Guillain
Barre Syndrome
 explain the nursing management of patient with
Guillain Barre Syndrome

6. NEURON

7. 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.

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

9. 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.

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

11. 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

12. 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

13. 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

14. 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.

15. 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.

16. 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.
.

17. 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.

18. 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

19. PATHOPHYSIOLOGY
Organisms /Trauma
Gangliosidosis-1 enters the nerves
and nodes of Ranvier
Anti GB1ab as a part of molecular mimicry
Complement mediated injury at para nodal
axon-glial junction
Disrupts the cluster of sodium channels
Conduction block

20. 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

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

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

23. 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.

24. 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).

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

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

27. 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

28. 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

29. 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

30. 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.