Mr. Husain Nadaf, Tutor

1. GUILLIAN BARRE
SYNDROME
GUIDED BY :
MR. AMOS TALSANDEKAR
ASSISTANT PROFESSOR
MEDICAL – SURGICAL NURSING
D.Y PATIL COLLEGE OF NURSING

2. INTRODUCTION
• Guillain-Barre syndrome is an autoimmune attack of 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 Movement hyporeflexia, and paresthesia's
(numbness).

3. DEFINITION
Autoimmune disorder affecting immune system and a part of
peripheral nervous system causing weakness of all muscle
-Lewis SL
Georges Guillain (1876–1961) and Jean
Alexandre Barré (1880–1967), French neurologists
Guillain barre syndrome is as serious condition in which it
mistakely affect a part of nervous system or body defense
mechanism that leads to degeneration and inflammation that
causes muscle weakness

4. INCIDENCE
• GBS annual incidence of 1.3 cases per population of 100 000,
with men being more frequently affected than women. GBS
is considered to be an autoimmune disease triggered by a
preceding bacterial or viral infection.

5. CAUSES
• Idiopathic
• Viral infection – AIDS,
herpes simplex virus
• Swine flu vaccination
• Hodgkin’s disease –
cancer of immune
system
• Certain medication like
immunosuppressive
agents
• General surgeries that
damages nerve

6. CLASSIFICATION
• Acute inflammatory demylenating polyneuropathy –
Commonest form of GB syndrome caused by direct
autoimmune response against Schwann cells (Cells that
produces the myelin sheath)
• Miller tiisue syndrome – Rare condition which affects eyes
causes ataxia and opthalmoplegia
• Acute motor axonal neuropathy – usually affects the motor
functions and impulse transmission

7. • Acute motor sensory axonal neuropathy – it affects
both motor and sensory functions
• Bickerstaff’s – Severe form of GBS that affects
sensory, motor and characterized by ataxia and
opthalmoplegia

8. PATHOGENESIS
• Due to etiological factor
• Immune response directed against capsular components that
produces antibodies
• Lymphocytes and macrophages that circulates in blood gets
affected
• followed by axonal damage
• defects in electrical impulse transmission motor and sensory
leads to weakness and parathesia

9. CLINICAL MANIFESTATION
• Pain in lower back
• Progressive muscle weakness
• Diminished muscle reflex
• Tingling sensation or numbness
• Palpitation in some cases
• Muscle spasm and ataxia
• Nystagmus – uncontrolled repetitive movements of eyes

10. DIAGNOSTIC EVALUATION
• History collection and physical examination
• CSF analysis
• EEG (electroencephalogram)
• PET scan

11. TREATMENT
• There is no known cure for GBS
• Intensive care includes the following features:
• Respiratory therapy
• Cardiac monitoring
• Safe nutritional supplementation
• Monitoring for infectious complications (eg, pneumonia,
urinary tract infections, septicemia)
• Prevention of thrombosis, pressure sores, and contractures
• Bowel and bladder management

12. • Mental status management
• Physical Therapy
• Occupational and Recreational Therapy – participation
in recreational therapy assists in the patient's
adjustment to disability and improves integration into
the community. Recreational activities, either new or
adapted, can be used to promote the growth,
development, and independence of a long-term
hospital patient.

13. • Speech Therapy - Speech therapy is aimed at
promoting speech and safe swallowing skills for
patients who have significant oropharyngeal weakness
with resultant dysphagia and dysarthria. In ventilator-
dependent patients, alternative communication
strategies also may need to be implemented.
• Immunotherapy - Plasma exchange carried out over a
10-day period may aid in removing autoantibodies

14. • Corticosteroids – Methylprednisolone, Substantial evidence
shows that intravenous methylprednisolone alone produces
neither significant benefit nor harm. In combination with
IVIG, intravenous methylprednisolone may hasten recovery
but does not significantly affect long-term outcome.
• Analgesia - Pain medications may be required in inpatient
and outpatient settings. A tiered pharmacologic approach that
starts with nonsteroidal anti-inflammatory drugs (NSAIDs) or
acetaminophen, with narcotic agents added as needed, is
usually recommended.
• Prevention of Thromboembolism

15. • Consultations - Consultation with a neurologist can be helpful
in the initial diagnosis, workup, and treatment of patients
admitted to the medical floor with GBS.Critical care
specialists may be required for patients in the ICU to help
manage respiratory failure and multiple medical
complications. Consultation with a pulmonologist may be
needed to perform workup and to manage respiratory issues,
such as acute respiratory distress syndrome (ARDS),
pneumonia, and respiratory failure.

16. NURSING MANAGMENT
• Watching for blood clots / DVT
• Monitor vital signs closely
• Keep patient safe from falls risks, considering that weakness
or paralysis may occur
• Provide pain management appropriate to the individual –
evidently, there will be a need to consider the types of
analgesics used and their potential side effects on the person
affected by GBS
• You may need to help the client to control their body
temperature

17. • Look for Complications of GBS can involve pneumonia and
respiratory failure – you may need to complete regular,
thorough observations and assessments (including respiratory
assessments) of the client
• Referral to other health professionals in the multidisciplinary
team e.g. physiotherapists to improve mobility and prevent
deformity
• Education to patient and family members or carers