Guillain-Barré syndrome is an acute inflammatory polyneuropathy that causes generalized paralysis. It is usually triggered by a viral or bacterial infection and causes the immune system to damage nerve cells. Common symptoms include progressive muscle weakness, numbness, and pain. Treatment involves immunotherapy to reduce immune response and support for breathing and other vital functions until recovery. Most patients recover fully but a small percentage have permanent nerve damage or die from respiratory failure.

2. GULLAIN BARRE
SYNDROME
Evaluator: Mr L Anand Presenter: Shruti Shirke
[Asso professor, CON AIIMS BBSR] M.Sc Neuroscience Nursing

3. Introduction
■ Guillain-Barré syndrome is an acute inflammatory
polyneuropathy that is the most common cause of acute or
subacute generalized paralysis.
■ It is caused by an autoimmune response to a viral infection. Most
patients give a history of a recent (i.e., 1 to 3 weeks) acute
infection, such as an upper respiratory infection, viral
pneumonia, or gastrointestinal (GI) infection.

4. Introduction cont..
■ A Campylobacter jejuni infection is often an antecedent to GBS.
In a few instances, the patient reports receiving a vaccination
prior to the onset of GBS.
■ As a result of improved respiratory management, most patients
survive. Most patients (75% to 85%) make a good recovery from
GBS, although 2% to 12% succumb to complications

5. Definition
■ Guillain-Barré syndrome is an acute inflammatory
polyneuropathy that is the most common cause of acute or
subacute generalized paralysis.
■ GBS is a rapidly evolving areflexic motor paralysis with or
without sensory disturbance.

6. Epidemiology
■ 0.4 to 2 cases per 100,000
■ Males are more affected than female

7. Etiology
Gastrointestinal and respiratory infections(camphylobactor jejuni)
Trauma and injury
Influenza infection
Influenza vaccine
1 case per 1 million vaccination
Surgery

9. Pathophysiology
■ Occurs in post-infection
■ Appear related to molecular mimicry
■ Ganglioside antibodies

13. Subtypes of Guillain-Barré Syndrome
■ Several subtypes of GBS based on pattern and symptoms of
peripheral nerve involvement.
■ The most common are acute inflammatory demyelinating
polyneuropathy (AIDP),
■ Acute motor axonal neuropathy (AMAN),
■ Acute motor sensory axonal neuropathy (AMSAN), and
■ Miller-Fisher syndrome (MFS).
■ Pharyngeal-Cervical-Brachial Variant (PCB)

14. Subtypes of Guillain-Barré Syndrome

15. AIDP
Reduced distal sensation
Frequent evidence of dysautonomia
Progressive symmetrical weakness
Elevated CSF protein without pleocytosis
Demylination
Muscle pain usually present
Decrease or absent conduction velocity

16. AMAN
Affects children and young adults
Identical to ascending GBS, except sensory
signs and symptoms are absent
May be a mild form of ascending GBS
Muscle pain is generally not present
Electrophysiologic diagnosis: axonal
involvement (decrease amplitude)

17. AMSAN
Affects mostly adults
Motor: initial weakness in the brainstem cranial nerves (facial, glossopharyngeal,
vagus, and hypoglossal nerves); then weakness progresses downward
Sensory: numbness occurs distally, more often in the hands than in the feet
Often rapid respiratory involvement
Electrophysiologic diagnosis: axonal involvement

18. Miller-Fisher Syndrome
■ Rare (5% of patients with GBS)
■ Affects adults and children
■ Seen as a triad of ophthalmoplegia, ataxia, and areflexia
■ Usually no sensory loss
■ Electrophysiologic diagnosis: demyelinating disease

19. Pharyngeal-Cervical-Brachial Variant
■ Rare
■ Isolated facial, oropharyngeal, cervical, and upper limb
weakness without lower limb involvement
■ Occurs with or without ptosis

20. Clinical features
Motor Sensory
Autonomic Cranial nerve

21. Clinical features In general: Motor
Motor weakness
(symmetric,
beginning in the legs
and progressing to
the trunk and arms)
flaccid paralysis Areflexia
Respiratory failure is
attributable to
mechanical failure
Fatigue of the
intercostals and
diaphragm.

22. Clinical features: CN
■ The facial (CN VII) nerve is most often affected: Inability to smile,
frown, whistle, or drink with a straw
■ Other cranial nerves that are less often affected are the
glossopharyngeal (CN IX) spinal accessory (CN XI), and hypoglossal
(CN XII) : Dysphagia and laryngeal paralysis can develop as a result
of paralysis of cranial nerves IX and X
■ Vagus(CN X): Vagus nerve deficit, if present, is thought to be
responsible for the autonomic dysfunction noted in some patients.

23. Clinical features In general: Sensory
■ Paresthesia: The paresthesia is
frequent and temporary and is
described as a tingling, “pins and
needles” feeling, a heightened
sensitivity to touch, or numbness.
Sensory changes are often noted
in the hands and feet (glove and
stocking distribution).

25. Clinical features In general: Sensory cont..
■ Pain: Pain is underrated in
terms of frequency and
intensity. The pain may begin as
cramping and progress to frank
pain in the arms, legs, back, or
buttock. Pain is often worse at
night and often interferes with
sleep

26. Clinical features: Autonomic symptoms
Cardiac arrhythmias
Paroxysmal hypertension
Orthostatic hypotension
Paralytic ileus
Urinary retention, or syndrome of inappropriate secretion of
antidiuretic hormone (SIADH)
GBS does not affect the level of consciousness, cognitive function, or
pupillary signs.

27. Clinical features
■ Acute: The acute stage begins with the onset of definitive
symptoms and ends when no additional symptoms or
deterioration are noted (lasts from 1 to 3 weeks).
■ In the plateau stage, the clinical presentation remains constant;
the time frame is a few days to a few weeks.
■ In the recovery stage, there is gradual improvement of signs
and symptoms over time. The recovery phase is synonymous
with the remyelination and axonal regeneration process.

28. Clinical course
Acute, chromic, recovery

30. Diagnosis: Clinical criteria
1. Progressive weakness of two or more limbs due to neuropathy (excluding
Miller-Fisher Syndrome).
2. Areflexia
3. Disease course less than 4 weeks
4. 4 A history of a recent viral infection
5. Elevated CSF protein levels with a normal cell count (albumin-cytologic
disassociation)
6. Abnormal EMG studies are seen
7. Nerve conduction velocities are slowed soon after paralysis develops

33. Diagnosis
NCS EMG
CSF
Analysis

34. Nerve conduction studies
■ Acute inflammatory demyelinating polyneuropathy: features of
demyelination (decreased motor nerve conduction velocity, prolonged
distal motor latency, increased F-wave latency, conduction blocks,
and temporal dispersion).
■ Acute motor axonal neuropathy: no features of demyelination (one
demyelinating feature in one nerve, if distal CMAP amplitude is less
than 10% LLN, can be found; distal CMAP amplitude less than 80%
LLN in at least two nerves.
■ Transient motor nerve conduction block might be present.

35. CSF Analysis
■ (CSF) is important especially to exclude other causes of weakness
associated with an increase in CSF cell count.
■ The disorder is classically known for its cytoalbuminological
dissociation—the combination of a normal cell count and increased
protein level. However, normal protein level (especially when
determined in the first week after onset of disease) does not make the
diagnosis unlikely or even exclude Guillain-Barré syndrome.
■ Additionally, 15% of patients with the disease have a mild increase in
CSF cell count (5–50 cells per μL

36. Management

38. Medical Management
■ Specific therapy with immunotherapy using either highdose
intravenous immunoglobulin (IV Ig), The IV Ig is usually given
on 5 sequential days for an overall dose of 0.4 g/kg of body
weight.
■ If the choice of therapy is plasmapheresis, 40 to 50 mL/kg
plasma exchange daily for 4 to 5 days is provided.
■ Some patients require a second course of treatments because of
relapse.

39. Respiratory Support.
■ Some patients will need to be intubated and supported temporarily on a
ventilator.
■ To avoid emergency intubation and the increased risk of aspiration, vital
capacity is monitored and compared with a predetermined optimal level for
the patient (approximately 12 to 15 mL/kg).
■ In a 160-pound person, the target vital capacity is about 1000 to 1200 mL.
When the patient’s vital capacity falls below this level, elective intubation and
mechanical ventilation may be indicated

40. Respiratory Support cont..
■ Pneumonia related to mechanical respiratory failure is a
common complication in these patients.
■ Some patients require ventilatory support for a short time (2
weeks). However, for those who require extended ventilation, a
tracheotomy is necessary
■ Stabilized and respiratory function has improved (as evidenced
by a vital capacity of 8 to 10 mL/kg), weaning from the
ventilator is begun.

41. Erasmus GBS Respiratory Insufficiency
Score (EGRIS)

45. Management of complication
Autonomic
Dysfunction
Sleep
Dysfunction
Pain
Nutrition Immobility

46. Management of complication
Autonomic Dysfunction
■ Placing the patient on a cardiac monitor is helpful in identifying
cardiac arrhythmias.
■ If paralytic ileus occurs, a nasogastric tube is inserted for gastric
decompression.
■ An intermittent catheterization program is instituted to relieve
urinary retention.
■ Fluid and electrolytes are monitored for imbalance caused by
SIADH.

47. Management of complication
Sleep Dysfunction
■ A disturbed sleep-wakefulness cycle leads to sleep deprivation.
■ Pain can interfere with sleep, although the altered sleep
patterns common to GBS patients
■ it contributes to the psychological stress experienced by the
patient.

48. Management of complication
Pain
■ Described as a “severe charley horse,”
■ The pain appears to be worse at night and is not relieved by
nonsteroidal anti-inflammatory agents or by nonnarcotic
agents.
■ Administering narcotics with a slow IV drip has yielded good
results.

49. Management of complication
Nutrition
■ Patients rapidly lose weight and muscle mass, leading to
weakness, fatigue, and failure to wean from a ventilator.
■ Nutritional support is aimed at beginning feeding as soon as is
appropriate for the patient.

50. Management of complication
Immobility
■ Emphasis should be on such nursing interventions as proper
nutrition and maintenance of skin integrity.
■ Minidoses of heparin are administered to prevent deep vein
thrombosis (DVT) and pulmonary emboli.
■ The use of compression boots for the prevention of DVTs is
controversial.

51. Nursing Management
■ Nursing management in the acute phase of GBS includes a
comprehensive baseline neurological and respiratory
assessment and ongoing monitoring for early recognition of
change. Assessment and ongoing monitoring include the
following:

52. Respiratory Focus
■ Assess respiratory rate and quality frequently.
■ Assess vital capacity frequently; know the predetermined value for
intubation.
■ Monitor the patient for respiratory insufficiency (e.g., air hunger,
abdominal breathing, cyanosis, diaphoresis, dyspnea, confusion, and
anxiety).
■ Monitor perfusion with pulse oximetry.
■ Administer oxygen as ordered.
■ Be prepared for the possibility of intubation.

53. Nursing Management cont..
Neurological Focus
■ Assess motor and sensory function frequently.
■ Assess cranial nerve function.
Autonomic dysfunction
■ Monitor for cardiac arrhythmias; vital signs indicating
hypotension or hypertension; and urinary retention.

54. Nursing diagnosis
■ The major patient problems and nursing diagnoses related to
the nursing management of patients with GBS include the
following:

55. Nursing diagnosis
Risk for Ineffective Breathing Pattern related to neuromuscular weakness of the respiratory
muscles (diaphragm and intercostals)
Ineffective Airway Clearance related to weakness of the cough reflex and the respiratory
muscles (diaphragm and intercostals)
Knowledge Deficit related to acute illness and hospitalization
Risk for Disuse Syndrome related to immobility secondary to paralysis and confinement of
ventilator
Impaired Verbal Communication related to paralysis of the muscles of speech or intubation
Pain related to peripheral nerve injury
Sleep Pattern Disturbance related to altered autonomic function and pain
Fear related to illness, hospitalization, treatment protocols, and death

56. Outcome and prediction of outcome
■ Guillain-Barré syndrome is still a life-threatening disorder with
frequent morbidities, even with the best treatment available.
Mortality rates in Europe and North America vary between 3%
and 7%, and more widely in other countries where data are
available.
■ 6 Patients can die in the acute progressive stage, most probably
because of ventilator insufficiency or pulmonary complications,
or from autonomic dysfunction including arrhythmia.

57. Guillain-Barré syndrome (GBS) Disability
Score

58. Research evidence
■ Guillain-Barré syndrome associated with SARS-CoV-2 infection:
causality or coincidence?
■ the onset of Guillain-Barré syndrome symptoms in this patient
overlapped with the period of SARS-CoV-2 infection. Hence
Guillain-Barré syndrome associated with SARS-CoV-2 might
follow the pattern of a parainfectious profile, instead of the
classic postinfectious profile, as reported in Guillain-Barré
syndrome associated with Zika virus

59. Summary

60. Conclusion
■ GBS is an acute inflammatory demyelinating polyneuropathy
characterized by progressive symmetric ascending muscle weakness,
paralysis, and hyporeflexia with or without sensory or autonomic
symptoms.
■ GBS is believed to result from autoimmune humoral and cell mediated
responses to a recent infection or any of a long list of medical problems.