Definition

Guillain-Barré is an autoimmune attack on the peripheral nerve myelin. It is an acute,

rapidly progressing and potentially fatal form of polyneuritis. It is also called postinfectous
polyneuropathy and ascending polyneuropathic paralysis. This disorders affects the peripheral
nervous system and results in loss of myelin and edema and inflammation of the affected nerves.
with adequate supportive care, 85% to 95% of these patients recover completely.

Pathophysiology

Myelin is a complex substance that covers nerves, providing insulation and speeding the
conduction of impulses from the cell body to the dendrites. The cell that produces myelin in the
peripheral nervous system is the Scwhann cell. In Guillain Barré, the schwann cells can be
spared, allowing for remyelination in the recovery phase of the disease. If damage has occurred
to the axons, then regrowth is required and takes months or years and is often incomplete.

Guillain-Barré syndrome is the result of cell-,ediated and humoral immune attack on

peripheral nerve myelin proteins that causes inflammatory demyelination. An infectious
organism contains an amino acid that mimics the peripheral nerve myelin protein. When this
organism enters the body, theimmune syytem cannot distinguish between the two proteins and
attacks and destroys the peripheral nerve myelin protein. With the auto immune attack, there is
an influx of macrophages and other immune-mediators agents that attack myelin and cause
inflammation and destruction, interruption of nerve conduction, and axonal loss. Muscles
innervated by the damaged peripheral nerves undergo denervation and atrophy.

Manifestations

1. Muscle weakness – weakness usually begins in the legs and may progresses upward.
Occurs over hours to days to weeks, usually peaking about 14 dy. Distal muscles are
more severely affected.
2. Neurologic manifestations
 Blindness – this is caused by demyelination of the optic nerve
 Bulbar muscle weakness – related to demyelination of the glossopharyngeal
 Inability to swallow and clear secretions –demyelination of vagus nerves
 Facial weakness and paresthesia – demyelination of facial nerves
 Extra ocular eye movement difficulties – demyelination of occulomotor nerves
and abducens
3. Autonomic dysfunction
 tachycardia, bradycardia, hypertension, or orthostatic hypotension – result of
demyelination of vagus nerves
 bowel and bladder dysfunction, facial flushing, and diaphoresis
4. Areflexia – absent of reflexes
 5. Paresthesia (numbness and tingling) – demyelination of sensory fibers. It is frequent and
usually follows in the extremities. Sensory loss is variable, with deep sensation more
affected than superficial sensations.
6. Pain – can be categorized as paresthesias, muscular aches and cramps, and
hyperesthesias. Pain appears to be worse at night. Pain may lead to decrease appetite and
interfere with sleep.

Diagnostic examinations

 Cerebrospinal fluid is normal or has low protein content initially, but after 7 to 10
days it shows a greatly elevated protein level (700 mg/dL)
 Electromyographic (EMG) and nerve conduction studies are markedly abnormal,
showing reduced nerve conduction velocity, in affected areas.

Management

1. Plasmapheresis – patient’s plasma and plasma components are removed through a

centrally placed large-bore double lumen catheter. The blood cells and antibody-
containing plasma are separated, after which the cells and a plasma substitute is
reinfused.
2. Intravenous administration of high-dose immunoglobulin (Sandoglobulin) - has been
effective as plasmapheresis and has the advantage of immediate availability and
safety. After 3 weeks past disease onset, plasmapheresis and immunoglobulin
therapies have little value.
3. Corticosteroid – have a little effect on the disease prognosis or duration
4. Vasopressors agents and volume expanders may be needed to treat low BP.
5. Opioids – may be indicated for those experiencing severe pain

Nursing Management

Nursing diagnosis: imbalanced nutrition; less than body requirements related to inability to
swallow.

Nursing inference: Due to the demyelination of the nerves, there will be impairment in the
transmission of impulses resulting to the decrease of stimulation in swallowing and bulbar
muscle weakness thus decreasing the amount of swallowed food.

Nursing intervention:

1. Gastrostromy tube is placed to administer nutrients.

2. Administration of IV fluids and parenteral nutrition
3. Assess for the return of gag reflex and bowel sounds before resuming oral nutrition.

References
1. Hinkle J.L. & Cheever K.H. (2014). Brunner and Suddarth’s textbook of Medical-
Surgical Nursing, 13th ed. Wolters Kluwer Health / Lippincott Williams & Wilkins.
2. Dirksen S. R., et. al. (2007). Medical-Surgical Nursing; assessment and management
of clinical problems, 7th ed. Mosby Inc.