Guillain–Barré Syndrome (GBS)
GBS, also known as acute idiopathic polyneuritis, is an
autoimmune attack on the peripheral nerve myelin
 rapid segmental demyelination of peripheral nerves
and some cranial nerves, producing ascending
weakness with dyskinesia (inability to execute
voluntary movements), hyporeflexia, and
paresthesias (a sensation of numbness, tingling, or a
“pins and needles” sensation).
Most common infectious agents that are associated with the
development of GBS.
 Campylobacter jejuni (implicated in 24% to 50% of
cases), cytomegalovirus, Epstein–Barr
virus,Mycoplasma pneumoniae, H. influenzae, and
HIV
Types of GBS
 With the most well-known type, the patient
experiences weakness in the lower extremities, which
progresses upward and has the potential for
respiratory failure.
 The second type is purely motor with no altered
sensation.
 Third type, called descending GBS, is much more
difficult to diagnose; it mostly affects the head and
neck muscles.
 The rarest type, the Miller–Fisher variant, presents
with ataxia, areflexia, and opthalmoplegia
P athop hysiology
GBS is the result of a cell-mediated and humoral immune
attack on peripheral nerve myelin proteins that causes
inflammatory demyelination.
 The immune system cannot distinguish between the
 two proteins and attacks and destroys peripheral
nerve myelin
 The exact location of the immune attack within the
peripheral nervous system is the ganglioside GM1b
 With the autoimmune attack, there is an influx of
macrophages and other immune-mediated agents
that attack myelin and cause inflammation and
destruction, interruption of nerve conduction, and
axonal loss
Clinical Manifestations
 Muscle weakness and diminished reflexes of the
lower extremities.
 Hyporeflexia and weakness may progress to
tetraplegia
 Sensory symptoms include paresthesias of the hands
and feet and pain related to the demyelination of
sensory fibers.
 Weakness usually begins in the legs and may
progresses upward.
 Maximum weakness (the plateau) varies in length but
usually includes neuromuscular respiratory failure and
bulbar weakness
GBS progresses to peak severity typically within 2 weeks and
no longer than 4 weeks. If progression is longer, then the
patient is classified as having chronic inflammatory
demyelinating polyneuropathy
Cranial nerve demyelination can result in a variety of clinical
manifestations. Optic nerve demyelination may result in
blindness.
Bulbar muscle weakness related to demyelination of the
glossopharyngeal and vagus nerves results in the inability to
swallow or clear secretions.
 Vagus nerve demyelination results in autonomic
dysfunction, manifested by instability of the
cardiovascular system
 The presentation is variable and may include
tachycardia, bradycardia, hypertension, or orthostatic
hypotension
There may be a sensory presentation, with progressive
sensory symptoms; an atypical axonal destruction; or the
Miller–Fisher variant, which includes paralysis of the ocular
muscles, ataxia, and areflexia
Assessment and Diagnostic Findings
 Changes in vital capacity and negative inspiratory
force are assessed to identify impending
neuromuscular respiratory failure.
 Serum laboratory tests are not useful in the diagnosis.
However, elevated protein levels are detected in CSF
evaluation, without an increase in other cells. Evoked
potential studies demonstrate a progressive loss of
nerve conduction velocity.
Medical Management
 Respiratory therapy or mechanical ventilation may be
necessary to support pulmonary function and
adequate oxygenation
 Elective intubation before the onset of extreme
respiratory muscle fatigue
 Emergent intubation may result in autonomic
dysfunction, and mechanical ventilation may be
required for an extended period
 anticoagulant agents and sequential compression
boots to prevent venous thromboembolism (VTE),
including deep vein thrombosis (DVT) and PE

TPE and IVIG are used to directly affect the peripheral nerve
myelin antibody level.

 Both therapies decrease circulating antibody levels

and reduce the amount of time the patient is
immobilized and dependent on mechanical ventilation
 electrocardiographic (ECG) monitoring

Tachycardia and hypertension are treated with short-acting

medications such as alpha-adrenergic blocking agents

 The use of short-acting agents is important, because

autonomic dysfunction is very labile
 Hypotension is managed by increasing the amount of
IV fluid administered.