Guillain-Barré syndrome is a rare autoimmune disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and paralysis. It is considered a post-infectious disorder, often triggered by bacterial or viral infections. Clinically, it begins with pain, paresthesia, and weakness in the legs that ascends to the trunk and arms. Diagnosis involves lumbar puncture showing elevated proteins with normal cell counts and electrodiagnostic testing showing demyelination. Treatment focuses on supportive care like ventilation and immunotherapy using plasma exchange or IVIG. Recovery can take many months but most experience significant improvement.

1. GUILLAIN-BARRÉ
SYNDROME
Ms Tarika Sharma
Assistant Professor
MMCON, MMU, Ambala

2. Introduction
Guillain-Barre syndrome is a rare but serious
autoimmune disorder in which the immune
system attacks healthy nerve cells of the
peripheral nervous system.

3. Introduction…
GBS is an acute inflammatory
demyelinating polyneuropathy that is the
most common cause of acute or subacute
generalized paralysis.
GBS is considered to be a postinfectious
immune-mediated disease targeting
peripheral nerves.

4. Definition
Guillain-Barre syndrome (GBS) is an acute
autoimmune disease marked by inflammation of
the peripheral nerves, affecting arms and legs and
Involves destruction of the myelin sheath
surrounding largest, most myelinated sensory and
motor fibers, resulting in disrupted
proprioception and weakness.

5. Normal Neuron

8. Epidemiology
1-2 (1.9) per 100,000 persons .
most commonly it affects young and middle-
aged adults 30 to 50 years of age.
Females slightly more affected than males.
More common in devloping countries.
Germany (7.9%), Mexico (44%), India (28%).

9. Etiology
The precise cause of Guillain-Barre is unknown. Sixty
percent of cases have followed a lung infection or a
gastrointestinal infection .
The following infections have been associated with
Guillain-Barre:
Campylobacter jejuni infection.
Influenza (the flu)
Cytomegalovirus (a strain of the herpes virus)
Epstein-Barr virus infection (mononucleosis)
Mycoplasma pneumonia
HIV

10. Triggers of GBS
Surgery
Trauma
Pregnancy
Hodgkin’s disease
HIV

11. PathophysiologyInfectious organism contains an
amino acid – mimics peripheral
nerve myelin protein.
Cell mediated immune attack on
peripheral nerve myelin protein
Immune system cannot
distinguish between the 2
proteins
Attack and destroys peripheral
nerve myelin
Inflammation and destruction of
myelin sheath
Axon is unable to support

12. Pathophysiology…
Specific immune response directed
against PNS antigen is initiated
Auto antigen T cells circulate & enter
the PNS
Auto antigen is recognised by T cells
Activation of local macrophages& B
cells to secrete auto antibodies

13. Cont..
Blood nerve barrier breaks down, leading
to entrance of specific auto antibodies
into nerve which cross react with myelin
Multifocal stripping of myelin
Defects in propagation of electrical nerve
impulses
Conduction block &flaccid paralysis

15. Disease Progression
80% experience complete recovery
Recovery may last from 2 months to 2 years
3 distinct phases:
Acute (4 wks) - initial rapid onset of symptoms
Plateu (few days to few weeks) - symptoms
neither worsen nor improve
Recovery - gradual improvement

16. Clinical Features
Initially Pain in the muscle
Weakness of muscle
The onset is gradual and progresses over days or weeks.
By the 3rd week 90% of the patient are weak.
Usually begins in the lower extremities and progressively
involves the trunk, the upper limbs, and finally the bulbar
muscles.
This pattern is known as Landry ascending paralysis.
Relatively symmetrically, but asymmetry is found in 9% of
patients
Paresthesias occur in some cases.

17. Clinical Features…
Respiratory insufficiency due to Intercostal and
diaphragmatic muscle paralysis
Dysphagia and facial weakness
Papilledema
oculomotor and other cranial neuropathies
The autonomic nervous system involvement:
lability of blood pressure and cardiac rate,
postural hypotension,
episodes of profound bradycardia
occasional asystole

18. Diagnosis
Physical Assessment, Vital signs (tachycardias,
bradycardias, Tachypnea, Blood pressure lability, bladder
retention, paralytic ileus)
Cranial nerves: Facial weakness, facial droop, dysphagia,
dysarthria,Ptosis from cranial nerve III (oculomotor) palsy
often is associated with limited eye movements.
Reflexes are absent or hyporeflexic, Pathologic reflexes,
such as Babinski, are absent.Hypotonia can be observed with
significant weakness

19. Lab Studies
CSF studies: During the acute phase of GBS
,an elevation in CSF protein (>0.55 g/L)
without an elevation of white blood cells (<10
lymphocytes/mL).
Complete blood counts
Serologic studies ( increase in titre for
infectious agent)

20. Diagnosis…
Electromyography (EMG) studies
Abnormalities in the NCS consistent with
demyelination are sensitive and represent
specific findings for classic GBS.
MRI
Pulmonary function tests
Histologic Findings:
Lymphocyte and macrophage infiltration is observed on
microscopic examination of peripheral nerves.

21. Treatment
Supporti
ve care
Ventilato
r support
Autonomic
dysfunctio
n
manageme
nt
Nutrition
al
support
Immune
therapy

22. Management…
Mechanical ventilation
Trachesotomy
Sustained hypertension
(ACE inhibitors, Beta blockers)
Postural hypotension
Urinary difficulties
Ventilator support
Autonomic dysfunction

23. Naso gastric tube
Hyperalimentation
Plasma exchange
Intravenous immunoglobulin
Nutritional support
Immune therapy
Management…

25. POTENTIAL COMPLICATIONS
Breathing difficulties
Heart and blood pressure problems
Residual numbness or other sensations
Pain
Bowel and bladder function problems
Blood clots
Pressure sores

26. Nursing management
Nursing Assessment
Assess pain level due to muscle spasms and
dysthesias.
Assess cardiac function including orthostatic
Blood Pressure.
Assess respiratory status closely to determine
hypoventilation due to weakness.
Perform cranial nerve assessment, especially ninth
cranial nerve for gag reflex.
Assess motor strength.

27. Nursing Diagnosis
Ineffective Breathing Pattern related to
weakness/paralysis of respiratory muscles
Impaired Physical Mobility related to
paralysis
Imbalanced Nutrition: Less Than Body
Requirements, related to cranial nerve
dysfunction

28. Cont…..
Impaired Verbal Communication related
to intubation, cranial nerve dysfunction
Chronic Pain related to disease pathology
Anxiety related to communication
difficulties and deteriorating physical
condition

29. Patient education
Advise patient and family that acute phase lasts 1 to 4
weeks, then patient stabilizes and rehabilitation can
begin; however, convalescence may be lengthy, from 3
months to 2 years.
Instruct patient in breathing exercises or use of
incentive spirometer to reestablish normal patterns.
Teach patient to wear good supportive and protective
shoes while out of bed to prevent injuries due to
weakness and paresthesia.

30. Cont….
Instruct patient to check feet routinely for
injuries because trauma may go unnoticed due
to sensory changes.
Reinforce maintenance of normal weight;
additional weight will further stress the motor
abilities.
Encourage the use of scheduled rest periods to
avoid over-fatigue.

31. Thank you….