Nursing

1. Prof. Mrs. Kavitha.P
Vice Principal
SUBJECT:
MEDICAL SURGICAL NURSING-II
UNIT NO:3
NURSING MANAGEMENT OF PATIENT WITH
NEUROLOGICAL DISORDERS
TOPIC:
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. 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.

4. 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

5. NEURON

6. 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.

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

8. 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.

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

10. 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

11. 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

12. 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

13. 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.

14. 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.

15. 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.
.

16. 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.

17. 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

18. 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

19. 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

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

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

22. 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.

23. 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).

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

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

26. 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

27. 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

28. 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

29. 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.