San Beda College – College of Nursing ORTHOPEDIC

NURSING

GUILLAIN – BARRЀ SYNDROME

I. Definition:
 Guillain-Barre syndrome is an
autoimmune disorder affecting peripheral
nervous system (PNS), usually triggered by
an acute infectious process.
 Disorder in which the body’s defense system
attacks its own body cells. The defense
system attacks myelin, the insulation
covering the nerves. The myelin is damaged
and nerve can’t send signals, which in turn
paralyzes the muscles.
 GBS is a demyelinating disease, meaning
that segments of myelin are stripped from
their insulating position around nerves,
reducing the propagation of electrical nerve
impulses.
 This causes loss of reflexes, muscle weakness, and temporary paralysis (loss of muscle
strength).
 characterized by the acute onset of peripheral and cranial nerve dysfunction
 This is a serious disorder because of the extent to which Nervous system is affected. The
cause is IDIOPATHIC but this is believed to be due to autoimmune, meaning the body’s
defense system attack its own body cells

II. Synonyms:

 Landry-Guillain-Barre syndrome; GBS; Acute idiopathic polyneuritis; Acute Inflammatory

Polyradiculoneuropathy ; Post-infectious Polyneuritis

III. Anatomy and Physiology:

NERVOUS SYSTEM
 The Nervous System consists of brain, spinal cord and complex network of neurons. This
system is responsible for sending, receiving and interpreting information from all parts of
the body.
 It monitors and coordinates internal organ function and responds to changes in external
environment
 This system can be subdivided into 2 parts - The CENTRAL and PERIPHERAL NERVOUS
SYSTEM. Let’s take a look at the Peripheral Nervous System:
FUNCTION: Controll of all motor, sensory, autonomic, cognitive and behavioral
activities.
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The NEURON
Functional Unit of the Nervous System
o Dendrites: receive neural messages and transmit towards cell body
o Axon: transmits neural messages away from cell body
o Cell body: contains nucleus, mitochondria ad other organelles
o Myelin Sheath produced by Schwann cells: Covering of axon, insulator and facilitate
conduction of neural impulses; fatty and protein material that surrounds certain nerve
fibers of brain and spinal cord
o glial cells forming the myelin sheaths are called oligodendrocytes in CNS while it is
called Schwann cells in PNS
o Rapid rate of conduction is called Saltatory Conduction
o Nodes of Ranvier: gaps between Myelin Sheath where saltatory conduction (jumping of
impulse between Myelin Sheaths) takes place

Types of Neurons:
• Sensory Neurons typically have long dendrites and short axon, carry messages
from sensory receptors → CNS
• Motor Neurons have a long axon and short dendrites, transmit messages from
CNS → muscles (or to glands)
• Interneurons are found only in CNS were they connect neuron to neuron
• Afferent Neurons: from tissues and organs into the CNS (sensory neurons)
• Efferent Neurons: from CNS to the effector cells (motor neurons

Peripheral Nervous System Divisions:

 The PNS is divided into following sections:
o Somatic NS – controls skeletal muscle as well as external sensory organs
o Autonomic NS – controls involuntary muscles, such as smooth and cardiac
muscles
 Sympathetic NS – controls activities that increase energy expenditures
 Parasympathetic NS - controls activities that conserve energy
expenditures

Peripheral Nervous System – nerves and ganglia outside the CNS

A.Nerve Structure and connective tissue sheath:

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Fiber – endoneurium
Fiber bundle/ Fascicle – perineurium
Nerve – epineurium
All Spinal nerves are mixed – sensory (afferent arm) and motor (efferent arm)

Spinal Cord – continuation of the brain stem; conduction pathway to and from the brain
covered by meninges; Major reflex center; gives rise to 31 pairs of Spinal nerves
Connection between the brain and periphery
Approx. → 45 cm (18 inches); thickness of the finger
 surrounded by a clear fluid called Cerebrospinal Fluid that acts like a cushion
 The nerves within the spinal cord are grouped together in different bundles called
Ascending and Descending tracts.
o Ascending tracts – carry information from the body, upward to the brain, such as
touch, skin temperature, pain and joint position.
o Descending tracts - carry information from the brain, downwards to initiate
movement and control body functions

NORMAL CSF FINDINGS

Pressure <20 cm H2O
Color/Appearance Clear, Colorless
Cells 0-5 small lymphocyte/mm2
Protein 15-45 mg/dl
Immune gamma 3-12% of total CHON
globulin (IgG)
Albumin/Globulin ratio 8:1
Glucose 50-75 mg/dl or 60-70% of
blood glucose level
Lactic acid 10-25 mg/dl

 Spinal Nerves / Nerve roots come off the spinal cord and pass out through a hole in
each of the vertebrae called Foramen to carry the information from the spinal cord to the
rest of the body, and from the body back up to the brain.
O Cervical Nerves “C” : nerves in neck; supply movement and feeling to the arms,
neck and upper trunk
O Thoracic Nerves “T”: nerves in upper back; supply trunk and abdomen
O Lumbar Nerves “L”, Sacral Nerves “S”: nerves in lower back; supply the legs,
bladder, bowel and sexual organs
SPINAL NERVES
Plexus Important Body Areas Served Result of Damage
Nerve
Cervical Phrenic nerve Diaphragm Respiratory paralysis
C1 – 5 Shoulders and neck muscles
Brachial Axillary nerve Deltoid muscle Paralysis
C5-8 T1
Radial nerve Triceps brachii, extensors of Wristdrop – inability to extend
forearm hand or wrist
Median nerve Flexors of forearm and hand Inability to pick up small
objects (pincer grasp)
Ape hand
Musculocutaneou Flexors of arm Inability to flex forearm or arm
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s
Ulnar nerve Wrist and hand muscles Claw hand – inability to spread
fingers apart
Lumbar Femoral nerve Lower abdomen, buttocks, Inability to extend leg and flex
L1-4 Ant. thighs, skin of anteromedial hip, loss of cutaneous
leg and thigh sensation
Obturator Adductor muscle of medial thigh Inability to adduct thigh
Skin of medial thigh and hip joint
Sacral Sciatic nerve Lower trunk, posterior thigh and Sciatica, inability to extend hip
L4-5 S1- leg and flex knee
4
Common Lateral aspect leg and foot Footdrop – inability to dorsiflex
peroneal / fibular the foot
Tibial nerve Posterior aspect leg and foot Shuffling gait – inability to
plantarflex and invert foot
Superior and Gluteus muscles Inability to extend hip
Inferior gluteal Inability to abduct and
nerve medially rotate the thigh

B.Cranial Nerves

CN Name Function Test

I Olfactory Purely sensory Sniffing different aromas
Carries Impulses for sense of smell
II Optic Purely sensory Eye chart and visual field testing
Carries impulses for vision Use of ophthalmoscope
III Oculomotor Motor fibers to eye muscles, Following moving objects
eyelid, lens Test for convergence; papillary
Controls pupil size/lens shape reflexes
IV Trochlear Motor fibers to the superior oblique Following moving objects
muscle
V Trigeminal Sensory fr. skin of face, nose and Sensation on face,corneal reflex
mouth testing, opening mouth against
Motor to chewing muscles resistance, moving jaw
VI Abducens Motor to lateral rectus muscle Following moving objects – lateral eye
movements
VII Facial Motor to muscles of facial Taste tongue for tastes – sweet, salty,
expression sour, bitter
to tear glands, salivary glands Close eyes, smile and whistle
Sensory fr. taste buds on anterior
tongue
VIII Vestibulococ Purely sensory – sense of balance Hearing test using tuning fork for
hlear (vestibular) and hearing (cochlear) bone and air conduction
Or Acoustic
IX Glossophary Motor to pharynx; swallowing and Gag reflex; swallowing and coughing
ngeal saliva production Test tongue for tastes
Sensory for taste buds – posterior
tongue
X Vagus Sensory and motor – pharynx, Gag reflex and swallowing
larynx, thoracic viscera coughing
Motor parasympathetic fibers –
regulate digestion and cardiac
activities
XI Accessory Motor to Sternocleidomastoid and Rotate head, shrug shoulders against
Trapezius resistance
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XII Hypoglossal Motor to tongue, sensory from Stick out tongue

tongue

IV. Pathophysiology:
Precipitating Factors:
Predisposing
Post infection of Campylobacter
Factors:
jejuni
Age (All ages)
Poor immunologic status
Sex – common in
Viral infection; CMV, EBV, VZV
males
Mycoplasma (bacteria that cause
PNM)
Post GIT and lung infection; Stress

Bacteria, other
viruses (e.g. C.
jejuni)

Enters the body by the use of

multifenestrated cells or other
mechanisms

Initiate immune response; activation of the CD4 T

cells and B cells that recognize the presence of
pathogens – this produces cell- mediated and
humoral response against the pathogen

Infectious organisms contain an amino

acid that mimics the peripheral nerve
myelin proteins

Molecular
Mimicry

Immune response directed against the capsular

components produce antibodies that cross-react
with myelin

Lymphocytes and macrophages

circulate in the blood and eventually
find myelin

The immune system cannot distinguish between

the two CHONs and attacks and destroys the
Peripheral Nerve Myelin

Lymphocytic infiltration of the spinal roots and

peripheral nerves and followed by macrophages-
mediated multifocal stripping of the myelin and
axonal damage
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Defects on the propagation of

electrical nerve impulses, with
Common: eventual conduction block Don’t affect
Typical GBS LOC/Cognitive
Function
GUILLAIN BARRЀ
SYNDROME

Sensory Changes: Acute progressive Dull aching pain of Cranial Nerve

• Paresthesia or ASCENDING the lower back, involvement:
numbness in feet WEAKNESS: flank, proximal legs • 7th, 9th & 10th CN
and hands -start from the legs d/t demyelination of  Difficulty forming
and progresses upward sensory fibers words (Dysarthria)
• lower limbs  Dysphagia
• upper limbs  Difficulty of
• hyporeflexia breathing,
• diminished reflexes speaking
 Blindness (optic
Demyelination of the nerve /CN 2
nerves that innervate damage)
the diaphragm and  Vagus nerve
intercostals muscles damage –
result in instability of CV
neuromuscular function; HPN,
respiratory failure

IF treated:
IF Not treated:
>Plasmapheresis Extensive axonal
>IVIG destruction
>Physical therapy
and exercise
>Medications Ascending weakness
progresses

GOOD PROGNOSIS Weakness of the

diaphragm and the
respiratory muscles

Respiratory Distress

BAD PROGNOSIS

Respiratory Arrest
Death
Shock
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V. Laboratory and Diagnostic Procedures:

Guillain-Barre syndrome can be difficult to diagnose in its earliest stages. Its signs
and symptoms are similar to those of other neurological disorders and may vary from
person to person.
 The first step in diagnosing Guillain-Barre syndrome is to take a careful medical
history to fully understand the cluster of signs and symptoms you're experiencing.
DIAGNOSTIC CRITERIA FOR GBS:
Features required for diagnosis -  Recovery beginning 2-4 wks after
 Progressive weakness of both legs progression ceases
& arms areflexia  Autonomic dysfunction
 Clinical features supportive of  Absence of fever at onset
diagnosis  Laboratory features supportive of
 Progression over days to 4 wks diagnosis
 Relative symmetry of signs  Elevated cerebrospinal fluid protein
 Mild sensory symptoms or signs with <10 cells/µl
 Cranial nerve involvement (bifacial  Electro diagnostic features of nerve
palsies) conduction slowing or block
 Spinal tap (lumbar puncture)
This procedure involves withdrawing a small amount of fluid from your spinal canal
at your low back (lumbar) level. This cerebrospinal fluid is then tested for a specific type of
change that commonly occurs in people who have Guillain-Barre syndrome.
A spinal tap (lumbar puncture) and nerve function tests are commonly used to help
confirm a diagnosis of Guillain-Barre syndrome.

 Nerve function tests

Your doctor may want information
from two types of nerve function tests —
electromyography and nerve conduction
velocity:
o Electromyography reads electrical
activity in your muscle to determine if
your weakness is caused by muscle
damage or nerve damage.
o Nerve conduction studies assess
how your nerves and muscles respond
to small electrical stimuli.
o A delay in F waves is present,
implying nerve root demyelination.
o Nerve motor action potentials may be decreased. This is technically difficult to
determine until the abnormality is severe.
o The extent of decreased action potentials correlates with prognosis.
 If Guillain-Barré syndrome is suspected, patients should be admitted to a hospital for
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electrodiagnostic testing,

CSF analysis, and monitoring by measuring forced vital capacity every 6 to 8 h.

Initial electrodiagnostic testing detects slow nerve conduction velocities and

evidence of segmental demyelination in 2/3 of patients; however, normal results do
not exclude the diagnosis and should not delay treatment.
 CSF analysis may detect albuminocytologic dissociation (increased protein >45
mg/dl but normal WBC count), but it may not appear for up to 1 wk and does not develop
in 10% of patients.
 MRI
o MRI is a sensitive but nonspecific test.
o Spinal nerve root enhancement with gadolinium is a nonspecific feature seen in
inflammatory conditions and is caused by disruption of the blood-nerve barrier.
o Selective anterior nerve root enhancement appears to be strongly suggestive of GBS.
o The cauda equine nerve roots are enhanced in 83% of patients.
 Forced vital capacity
o Forced vital capacity (FVC) is very helpful in guiding disposition and therapy.
o Patients with an FVC less than 15-20 mL/kg, maximum inspiratory pressure less than
30 cm H2 O, or a maximum expiratory pressure less than 40 cm H2 O generally
progress to require prophylactic intubation and mechanical ventilation.
 Many different abnormalities may be seen on ECG, including second-degree and third-
degree atrioventricular (AV) block, T-wave abnormalities, ST depression, QRS widening,
and a variety of rhythm disturbances.

VI. Medical-Surgical Management:

a. Plasmapheresis. AKA Plasma Exchange, is used to remove proteins, called
antibodies, from the blood. The process involves taking blood from the body, usually from
the arm, pumping it into a machine that removes the antibodies, then sending it back into
the body.
o type of "blood cleansing" in which damaging antibodies are removed from your
blood.
o removing the liquid portion of your blood (plasma) and separating it from the actual
blood cells. The blood cells are then put back into your body, which manufactures
more plasma to make up for what was removed.
o plasmapheresis rids plasma of certain antibodies that contribute to the
immune system attack on the peripheral nerves.
o helps when done early in the syndrome; it is used if γ-globulin is ineffective.
Plasmapheresis is relatively safe, shortens the disease course and hospital stay, and
reduces mortality risk and incidence of permanent paralysis. Plasmapheresis removes
any previously administered γ-globulin, negating its benefits.
b. Intravenous immunoglobulin. Immunoglobulin contains healthy antibodies
from blood donors. High doses of immunoglobulin can block the damaging antibodies that
may contribute to Guillain-Barre syndrome.

o used to reduce the severity and length of Guillain-Barre symptoms.

o the immunoglobulins are added to the blood in large quantity, blocking the
antibodies that cause inflammation; promote remyelination
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c. If the diaphragm is week, breathing support or even a breathing tube and mechanical
ventilator may be needed. – ptx. is weaned in when spontaneous respiration is
established.
d. Pain is treated aggressively with anti-inflammatory medicines and
narcotics, if needed.
e. Proper body positioning or a feeding tube may be used to prevent choking during feeding
if the muscles for swallowing are weak.
f. Anticoagulant may be used to prevent blood clots. – heparin as DVT prophylaxis.
g. Intubation should be performed on patients who develop any degree of
respiratory failure. Clinical indicators needed for intubation: hypoxia, rapidly
declining respiratory function, poor or weak cough, and suspected aspiration.
Typically, intubation is indicated when the FVC is less than 15 mL/kg.
h. Monitor closely for changes in blood pressure, heart rate, and other arrhythmias.
o Treatment rarely is needed for tachycardia. But may give Digitalis, Ca+ Channel
Blockers, VND drugs – Verapamil, Nefedipine, Diltiazem and Beta blockers , OLOL
drugs- Atenolol, Nadolol, Metoprolol
o Atropine is recommended for symptomatic bradycardia. (may also use
Isoproterenol)
o Because of the lability of dysautonomia, hypertension is best treated with short-acting
agents, such as a short-acting beta-blocker or nitroprusside (peripheral
vasodilator).
o Hypotension of dysautonomia usually responds to intravenous fluids and
supine positioning.
o Temporary pacing may be required for patients with second-degree and third-degree
heart block.

VII. Nursing Management:

 Monitor Vital Signs, esp. BP and HR to  Prevent complications of immobility
identify autonomic dysfunction; vital o Skin Care
capacity, breath sounds, and ABG o Padding may be placed at the
 Keep airway and tracheostomy set at the bony prominences
bed side o ROM exercises
 Suction, provide emotional support to the o Position changes
client and family because of the severity o Coughing and deep breathing
and lengthy convalescent period exercises
 If patient can’t swallow due to bulbar o Antiembolism stockings
paralysis (immobility of muscles),  Provide explanations of disease process
gastrostomy tube may be placed to and care
administer nutrients  Encourage client to verbalize feelings
 Assess return of gag reflex and bowel
sound before resuming oral nutrition