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GuillainBarr syndrome (GBS) results in the acute, rapid segmental demyelination of peripheral
nerves and some cranial nerves, producing ascending weakness with dyskinesia (inability to eecute
voluntary movements), hypore!eia and paresthesias (numbness)" GBS is an acute peripheral neuropathy
because it evolves over days to weeks" #s with other neuropathies, GBS may be aonal, demyelinating, or
#lmost a century ago, the $rench neurologists Guillain, Barr, and Strohl described two soldiers who
developed acute paralysis with are!eia that spontaneously recovered" %hey reported the combination of
increased protein concentration with a normal cell count in the &S$, or albuminocytological dissociation,
which di'erentiated the condition from poliomyelitis" (espite the fact that )andry had already reported
similar cases in *+,-" %he combination of these clinical and laboratory features became known as Guillain.
Barr syndrome (GBS)" /ntil now, GBS has remained a descriptive diagnosis of a disorder for which there
are no speci0c diagnostic tests" %he combination of rapidly progressive symmetrical weakness in the arms
and legs with or without sensory disturbances, hypo!eia or are!eia, in the absence of a &S$ cellular
reaction, remains the hallmark for the clinical diagnosis of GBS"
%he human nervous system consists of the brain and spinal cord, referred to collectively as the
central nervous system (&1S), and the nerves that etend into the head, trunk, and limbs, known as the
peripheral nervous system" #t the point where the peripheral nerves 0rst emerge from the spinal cord,
they are known as nerve roots or radicles" (amage to a nerve root is called radiculopathy" 2eripheral
nerves consist of bundles of hundreds of individual nerve 0bers, each smaller than a human hair" %hey
transmit electrical impulses, allowing the brain to keep in touch with all aspects of bodily function" Sensory
nerve 0bers send messages from peripheral structures, such as the skin, 3oints, and bones, to the brain"
4otor 0bers send messages from the brain to the muscles" %hese messages are sent in the form of
electrical impulses" 5ach nerve 0ber consists of an electrical cable known as an aon, and an insulating
sheath known as the myelin" %he myelin sheath is not a continuous structure, but consists of multiple
segmentsof myelin, each separated by a short gap known as the node of Ranvier. %he node of 6anvier is
where the electrical current is generated and renewed"
Peripheral neuropathyalso known as polyneuropathy or simply neuropathyis the term used to
describe any disorder of peripheral nerves" 2eripheral neuropathy that results primarily from the
degeneration of aons is known as an aonal neuropathy" (emyelinating neuropathy results from
degeneration of the myelin" 7n almost all neuropathies there is a combination of aonal degeneration and
GBS is an acute peripheral neuropathy because it evolves over days to weeks" #s with other
neuropathies, GBS may be aonal, demyelinating, or mied"
7n 5urope, 1orth #merica, and other developed countries, GBS is most commonly a demyelinating
neuropathy, and is known as acute in!ammatory demyelinating polyneuropathy (#7(2)" 7n this form of
GBS, the immune attack is directed against the myelin, causing loss of the myelin sheath and leading to a
8short circuit9 so that electrical messages cannot travel between the brain and the periphery of the body"
%here can be secondary damage to the aons in #7(2, but sometimes the primary immune.mediated
attack is against the aon itself, causing the electrical cable to degenerate" %his is called axonal GBS, and
it does occur in developed countries, but is uncommon" #7(2 is still the most common form of GBS in
developing countries, but the aonal form is relatively more common than it is in developed countries" GBS
is sometimes called a polyradiculoneuropathy because there is a predilection for the demyelination to
a'ect the nerve roots where they 0rst emerge from the spinal cord" 7n some cases of aonal GBS, the
attack is limited to the motor aons that control muscle activity" %his is called acute motor axonal
neuropathy (#4#1)" %his form of GBS causes only weakness, with no involvement of sensation" :hen
aonal GBS a'ects both sensory and motor functions, it is known as acute motor and sensory axonal
neuropathy (#4S#1)" #4S#1 is probably a more severe form of #4#1" 7t is commonly seen as summer
outbreaks in children in northern rural &hina" :hen there is etensive aonal degeneration, whether the
secondary aonal degeneration of #7(2 or the primary aonal degeneration of #4#1 or #4S#1, recovery is
slower and there is a greater likelihood of some residual weakness"
;ccasionally, GBS causes paralysis of the eye muscles and loss of balance and coordination" %his
condition is known as Miller Fisher syndrome (MFS), also known as the $isher syndrome" %hus, GBS is not a
single disease, but a group of disorders consisting of #7(2, #4#1, #4S#1, 4$S, and other rare variants"
Classifcation o GBS
Ac!t" in#a$$ato%& '"$&"linatin( )ol&%a'ic!lon"!%o)at*& +AIDP,
#ntibody mediated autoimmune disorder"
%riggered by antecedent infection or vaccination"
7n!ammatory demyelination present and may be accompanied by aonal nerve loss"
6emyelination occurs upon cessation of immune reaction"
Ac!t" $oto% a-onal n"!%o)at*& +AMAN,
4ost patients seropositive for &ampylobacter infection"
2ure motor aonal form of neuropathy"
2ediatric patients mostly a'ected and recovery typically rapid
Ac!t" $oto% s"nso%& a-onal n"!%o)at*& +AMSAN,
(egeneration of myelinated motor and sensory 0bers with minimal in!ammation and
Similar to #4#1 ecept #4S#1 only a'ects sensory nerves and roots"
%ypically a'ects adults"
Mill"% .is*"% s&n'%o$"
6are, rapidly evolving ataia, are!eia, with limb weakness and ophthalmoplegia"
Sensory loss not common, but proprioception can be impaired"
(emyelination and in!ammation of cranial nerves 777<7=, spinal ganglia, and peripheral nerves"
6esolution in one to three months"
Ac!t" )ana!tono$ic n"!%o)at*&
6arest of all types, with sympathetic, parasympathetic, and cardiac involvement"
6ecovery is gradual and incomplete
GBS is considered to be a postinfectious, immune.mediated disease targeting peripheral nerves" /p
to two thirds of patients report an antecedent bacterial or viral illness prior to the onset of neurologic
symptoms" 6espiratory infections are most fre>uently reported, followed by gastrointestinal infections"
#dministration of certain vaccinations and other systemic illnesses have also been associated with GBS"
&ase reports eist regarding numerous medications and procedures? however, whether any causal link
eists is unclear"
Ca$)*&lo/act"% 0"0!ni
7n several studies, C jejuni was the most commonly isolated pathogen in GBS" Gastrointestinal and
upper respiratory tract symptoms can be observed with C jejuni infections" 2atients who develop GBS
following an antecedent C jejuni infection often have a more severe course, with rapid progression and a
prolonged, incomplete recovery" # strong clinical association has been noted between C jejuni infections
and the pure motor and aonal forms of GBS"
&ytomegalovirus (&4=) infections are the second most commonly reported infections preceding
GBS, with &4= being the most common viral trigger of GBS" &4= infections present as upper respiratory
tract infections, pneumonias, and nonspeci0c, !ulike illnesses" GBS patients with preceding &4= infections
often have prominent involvement of the sensory and cranial nerves" &4= infections are signi0cantly
associated with antibodies against the ganglioside G4@"
Ot*"% in"ctions
;ther signi0cant, although less fre>uently identi0ed, infectious agents in GBS patients
include E)st"in-Ba%% 1i%!s (5B=), Mycoplasma pneumoniae, and 1a%ic"lla-2ost"% 1i%!s"

association between GBS and acute *!$an i$$!no'"fci"nc& 1i%!s (A7=) infection also is well

7nfections with Haemophilus infuenzae, Borrelia burgdorferi, para.in!uenBa virus type *,
in!uenBa # virus, in!uenBa B virus, adenovirus, and herpes simple virus have been demonstrated in
patients with GBS, although not more fre>uently than they have in controls"

GBS can also follow certain types of vaccination" %he best.known eample is the association of GBS
with the /"S" swine in!uenBa vaccination program of *-CD" 7n the fall of that year, approimately ,E million
people in the /nited States were vaccinated with a vaccine containing A!e" #ersey s"ine in$uen%a virus
in a program sponsored by the federal government" %here was an increase in the fre>uency of GBS in the
people who received the vaccine during the months that followed" Between ;ctober *, *-CD, and Fanuary
G*, *-CC, there were *,E-+ cases reported to the &enters for (isease &ontrol and 2revention (&(&)" ;f
these, ,G@ had received the vaccine prior to the onset of GBS" %his represented a more than @E.fold
increase in the number of cases epected to occur in nonvaccinated individuals" $urthermore, a
subse>uent vaccination program between *-C+ and *-C-, using a vaccine that did not contain swine
in!uenBa virus, caused no increase in the epected incidence of GBS" %hus, the *-CD outbreak appears to
have been speci0c for this particular vaccine"
GBS may possibly occur following vaccination for polio" (uring *-+,, following an outbreak of polio
in $inland, -H percent of the population was vaccinated over a ,.week period" 7n one district in southern
$inland, there was a marked increase in the number of GBS cases seen over the net H months" %here have
been no other reports of GBS following polio vaccination"
%he 0rst reports of GBS following vaccination appeared in the nineteenth century" Shortly after the
introduction of rabies vaccination by 2asteur in the late *+-Es, there were neurologic complications,
including acute polyneuritis" %his complication was related to contamination of the vaccine with nerve
tissue, but it has virtually disappeared in those areas of the world where the vaccine is prepared from duck
or chick embryos"
6ecently, there appear to be an increased risk for the general population? nor is there any risk that
people who have had GBS will relapse if they are vaccinated have been reports of GBS after vaccination
against the menin&ococcal 'acterium, which causes a form of meningitis" 7n @EE,, 0ve people developed
GBS a few weeks after receiving the vaccine" 7t is not known eactly how many people received this
particular vaccine, and therefore it is impossible to determine whether this represents a signi0cantly
increased risk" Aowever, the cases occurred @ to H weeks after receiving the vaccine, strongly suggesting
that the vaccine was the trigger"
# study by #li indicated that antibiotic therapy with !uoro>uinolones also is associated with the
development of GBS" /sing cases reported between *--C and @E*@ to the /S $ood and (rug
#dministration ($(#) #dverse 6eporting System, he determined that of ,G- reports of peripheral
neuropathy associated with !uoro>uinolone treatment, -I were for patients with GBS"
Ot*"% associations
=arious events, such as surgery, trauma, and pregnancy, have been reported as possible triggers of
GBS, but these associations remain mostly anecdotal" &ase reports cite associations between bariatric and
other gastric surgeries, renal transplantation, and epidural anesthesia" #necdotal associations include
systemic lupus erythematosus, sarcoidosis, lymphoma, and snakebite"
%umor necrosis factoralpha polymorphisms with increased epression are associated with many
autoimmune and in!ammatory diseases, and may increase susceptibility to aonal GBS subtypes"
Aowever, the role of these polymorphisms in GBS remains unclear and warrants further investigation"
%he typical patient with Guillain.Barr syndrome (GBS), which in most cases will be acute
in!ammatory demyelinating polyradiculoneuropathy (#7(2), presents @.H weeks following a relatively
benign respiratory or gastrointestinal illness with complaints of 0nger dysesthesias and proimal muscle
weakness of the lower etremities" %he weakness may progress over hours to days to involve the arms,
truncal muscles, cranial nerves, and muscles of respiration" =ariants of GBS may present as pure motor
dysfunction or acute dysautonomia"
%he mean time to the clinical function nadir is *@ days, with -+I of patients reaching a nadir by H
weeks" # plateau phase of persistent, unchanging symptoms then ensues, followed days later by gradual
symptom improvemet" 6ecovery usually begins @.H weeks after the progression ceases" %he mean time
to clinical recovery is @EE days"
%he classic clinical picture of weakness is ascending and symmetrical in nature" %he lower limbs are
usually involved before the upper limbs" 2roimal muscles may be involved earlier than the more distal
ones" %runk, bulbar, and respiratory muscles can be a'ected as well"
2atients may be unable to stand or walk despite reasonable strength, especially when
ophthalmoparesis or impaired proprioception is present" 6espiratory muscle weakness with shortness of
breath may be present" :eakness develops acutely and progresses over days to weeks" Severity may
range from mild weakness to complete tetraplegia with ventilatory failure"
C%anial n"%1" in1ol1"$"nt
&ranial nerve involvement is observed in H,.C,I of patients with GBS" &ranial nerves 777.=77 and 7J.
J77 may be a'ected" &ommon complaints include the followingK
$acial droop (may mimic Bell palsy)
2upillary disturbances
$acial and oropharyngeal weakness usually appears after the trunk and limbs are a'ected" %he
4iller.$isher variant of GBS is uni>ue in that this subtype begins with cranial nerve de0cits"
S"nso%& c*an("s
4ost patients complain of paresthesias, numbness, or similar sensory changes" Sensory symptoms
often precede the weakness" 2aresthesias generally begin in the toes and 0ngertips, progressing upward
but generally not etending beyond the wrists or ankles" )oss of vibration, proprioception, touch, and pain
distally may be present" Sensory symptoms are usually mild" 7n most cases, ob3ective 0ndings of sensory
loss tend to be minimal and variable"
2ain is most severe in the shoulder girdle, back, buttocks, and thighs and may occur with even the
slightest movements" %he pain is often described as aching or throbbing in nature"
(ysesthetic symptoms are observed in approimately ,EI of patients during the course of their
illness" (ysesthesias fre>uently are described as burning, tingling, or shocklike sensations and are often
more prevalent in the lower etremities than in the upper etremities"
;ther pain syndromes in GBS include the followingK
4yalgic complaints, with cramping and local muscle tenderness
=isceral pai1
2ain associated with conditions of immobility (eg, pressure nerve palsies, decubitus ulcers)
A!tono$ic c*an("s
#utonomic nervous system involvement with dysfunction in the sympathetic and parasympathetic
systems can be observed in patients with GBS"#utonomic changes can include the followingK
$acial !ushing
2aroysmal hypertension
;rthostatic hypotension
#nhidrosis and<or diaphoresis
/rinary retention due to urinary sphincter disturbances may be noted" &onstipation due to bowel
paresis and gastric dysmotility may be present" Bowel and bladder dysfunction are rarely early or
persistent 0nding" (ysautonomia is more fre>uent in patients with severe weakness and respiratory failure"
#utonomic changes rarely persist in a patient with GBS"
R"s)i%ato%& in1ol1"$"nt
/pon presentation, HEI of patients have respiratory or oropharyngeal weakness" %ypical complaints
include the followingK
(yspnea on eertion
Shortness of breath
(iLculty swallowing
Slurred speech
=entilatory failure with re>uired respiratory support occurs in up to one third of patients at some
time during the course of their disease"
S"%olo(ic St!'i"s
Serologic studies are of limited value in the diagnosis of GBS" #ssays for antibodies to the following
infectious agents may be consideredK
( )e)uni
&ytomegalovirus (&4=)
5pstein.Barr virus (5B=)
Aerpes simple virus (AS=)
Mycoplasma pneumonia
#n increase in titers for infectious agents, such as &4=, 5B=, or Mycoplasma, may help in
establishing etiology for epidemiologic purposes" A7= has been reported to precede GBS, and serology
should be tested in high.risk patients to establish possible infection with this agent"
S"%!$ a!toanti/o'i"s
Serum autoantibodies are not measured routinely in the workup of GBS, but results may be helpful
in patients with a >uestionable diagnosis or a variant of GBS" #ntibodies to glycolipids are observed in the
sera of DE.CEI of patients with GBS during the acute phase, with gangliosides being the ma3or target
Speci0c antibodies found in association with GBS include the followingK
#ntibodies to G4*K $re>uently found in the sera of patients with the acute motor aonal neuropathy
(#4#1) or acute demyelinating polyradiculoneuropathy (#7(2) variants of GBS
#nti.G4* antibodiesK 5levated titers are closely associated antecedent ( )e)uni infections
#nti.GM*b antibodiesK $ound in patients with GBS with ophthalmoplegia, including patients with the
4iller.$isher variant
;ther antibodies to di'erent ma3or and minor gangliosides also have been found in GBS patients"
L!$/a% P!nct!%"
4ost, but not all, patients with GBS have an elevated &S$ protein level (NHEE mg<)), with normal
&S$ cell counts" #n elevated &S$ protein concentration (with normal cell count) is only found on initial &S$
analysis in ,EI of patients? elevated &S$ protein concentration occurs in more than -EI of patients at
clinical nadir" &S$ protein may not rise until *.@ weeks after the onset of weakness
N!%sin( I$)lications5
*" ;btain a history of the patientOs complaints, including a list of known allergens, especially allergies
or sensitivities to late or anesthetics"
@" 6eview the procedure with the patient" 7nform the patient that the procedure will be performed by a
health care provider (A&2) trained to perform the procedure and takes approimately @E min"
#ddress concerns about pain and eplain that there may be some discomfort during the lumbar
puncture" 7nform the patient that a stinging sensation may be felt as the local anesthetic is in3ected"
7nstruct the patient to report any pain or other sensations that may re>uire repositioning of the
spinal needle"
G" 4ake sure a written and informed consent has been signed prior to the procedure and before
administering any medications"
,. 6ecord baseline vital signs, and assess neurologic status"
-. %o perform a lumbar puncture, position the patient in the knee.chest position at the side of the bed"
2rovide pillows to support the spine or for the patient to grasp" %he sitting position is an alternative"
7n this position, the patient must bend the neck and chest to the knees"
.. 2repare the site (usually between )G and )H or )H and ),) with povidone.iodine, and drape the area"
/. # local anesthetic is in3ected" /sing sterile techni>ue, the A&2 inserts the spinal needle through the
spinous processes of the vertebrae and into the subarachnoid space" %he stylet is removed" &S$
drips from the needle if it is properly placed"
0. ;btain &S$, and place in specimen tubes" %ake a 0nal pressure reading, and remove the needle"
&lean the puncture site with an antiseptic solution, and apply a small bandage"
,. #fter lumbar puncture, monitor vital signs and neurologic status every *, min for * hr, then every @
hr for H hr, and as ordered" %ake the temperature every H hr for @H hr"
-. #dminister !uids, if permitted, to replace lost &S$ and help prevent or relieve headache, which is a
side e'ect of lumbar puncture
.. 2osition the patient !at, either on the back or abdomen, although some A&2s allow GE degrees of
elevation" 4aintain this position for + hr" &hanging position is acceptable as long as the body
remains horiBontal.
N"%1" Con'!ction St!'i"s
%he nerve conduction study (1&S) is the most important part of electrodiagnostic testing in people
with GBS" 1&S is also known as 2lectroneuro&raphy (51G)" 7t is performed to identify peripheral nerve
in3ury, to di'erentiate primary peripheral nerve pathology from muscular in3ury, and to monitor response
of the nerve in3ury to treatment" # stimulus is applied through a surface electrode over a nerve" #fter a
nerve is electrically stimulated proimally, the time for the impulse to travel to a second or distal site is
measured" 1erve conduction studies are commonly done in con3unction with electromyelography? the
combination of the procedures is known as electromyoneuro&raphy.
Signs of demyelination can include the followingK
1erve conduction slowing
2rolongation of the distal latencies
2rolongation or absence of the $.waves
&onduction block or dispersion of responsesK 5vidence fre>uently demonstrated at sites of
natural nerve compression"
1ursing 7mplications
,. 7nform the patient the procedure is performed to measure electrical activity of the muscles"
-. 6eview the procedure with the patient" #ddress concerns about pain related to the procedure and
inform the patient the procedure may be uncomfortable because of a mild electrical shock" #dvise
the patient that the electrical shock is brief and is not harmful" 7nform the patient the procedure is
performed in a special laboratory by a health care provider (A&2) and takes approimately *, min
to complete, but can take longer depending on the patientOs condition"
.. Ma3e sure a "ritten and informed consent has 'een si&ned prior to the procedure and 'efore
administerin& any medications
*" 5nsure the patient has removed all eternal metallic ob3ects from the area to be eamined prior to
the procedure"
@" 7nstruct the patient to void prior to the procedure and to change into the gown, robe, and foot
coverings provided"
G" 2lace the patient in a supine or sitting position, depending on the location of the muscle to be
H" #pply electrode gel and place a recording electrode at a known distance from the stimulation point"
," %he nerve is electrically stimulated by a shock.emitter device? the time between nerve impulse and
electrical contraction, measured in millisec (distal latency), is shown on a monitor"%he nerve is also
electrically stimulated at a location proimal to the area of suspected in3ury or disease"
*" :hen the procedure is complete, remove the electrodes and clean the skin where the electrodes
were applied"
@" 4onitor electrode sites for in!ammation"
G" 7f residual pain is noted after the procedure, instruct the patient to apply warm compresses and to
take analgesics, as ordered"
2atients who are diagnosed with GBS should be admitted to a hospital for close monitoring until it
has been determined that the course of the disease has reached a plateau or undergone reversal"
#lthough the weakness may initially be mild and nondisabling, symptoms can progress rapidly over 3ust a
few days" &ontinued progression may result in a neuromuscular emergency with profound paralysis,
respiratory insuLciency, and<or autonomic dysfunction with cardiovascular complications"
R"s)i%ato%& t*"%a)&
#pproimately one third of patients with GBS re>uire ventilatory support" 4onitoring for respiratory
failure, bulbar weakness, and diLculties with swallowing help to anticipate complications" 2roper
positioning of the patient to optimiBe lung epansion and secretion management for airway clearance is
re>uired to minimiBe respiratory complications"
Serial assessment of ventilatory status is needed, including measurements of vital capacity and
pulse oimetric monitoring" 6espiratory assistance should be considered when the epiratory vital capacity
decreases to less than *+ m)<kg or when a decrease in oygen saturation is noted (arterial 2;@ P CE mm
Ag)" %racheotomy may be re>uired in a patient with prolonged respiratory failure, especially if mechanical
ventilation is re>uired for more than @ weeks"
Ca%'iac Monito%in(
&lose monitoring of heart rate, blood pressure, and cardiac arrhythmias allows early detection of
life.threatening situations" &ritically ill patients re>uire continuous telemetry and close medical supervision
in an 7&/ setting"

#ntihypertensives and vasoactive drugs should be used with caution in patients with
autonomic instability" Aemodynamic changes related to autonomic dysfunction are usually transitory, and
patients rarely re>uire long.term medications to treat blood pressure or cardiac problems"
P%"1"ntion o t*%o$/osis6 )%"ss!%" so%"s6 an' cont%act!%"s
2revention of secondary complications of immobility is also re>uired" Subcutaneous unfractionated
or low Q molecular.weight heparin ()4:A) and thromboguards are often used in the treatment of immobile
patients to prevent lower.etremity deep venous thrombosis ((=%) and conse>uent pulmonary
embolism (25)"
2revention of pressure sores and contractures entails careful positioning, fre>uent postural
changes, and daily range.of.motion (6;4) eercises"
Mana("$"nt o D&sa!tono$ia
#cute dysautonomia is a signi0cant cause of death in patients with GBS" &ardiac and hemodynamic
disturbance manifesting as hypertension, postural hypotension, and tachycardia occur in a ma3ority of GBS
patients"%his is due to ecessive sympathetic over activity and parasympathetic under activity" %achycardia
is most common, usually in the range of *EE*@E<min, which does not re>uire treatment"
#pproach to inserting a pacemaker for serious bradycardia or sinus arrest has varied widely
because of the uncertainty that eists in anticipating such events at the bed side by di'erent
ways"Aypertension is seen in one third of patients with GBS and can be labile or be followed by
hypotension" 7f hypertension is severe (mean pressure greater than approimately *@, mmAg) and
sustained, speci0c therapy may be necessary" #ntihypertensives with short half.lives (labetolol, esmolol, or
nitroprusside infusions) should be considered" Beta.adrenergic or calcium channel blockers should be used
with caution, especially if episodes of hypertension alternate with hypotension"
Aypotension can be managed by maintaining intravascular volume and avoid using diuretics"
2atients with a risk of hypotension should not be left unattended in a sitting or upright position"
2ronounced and persistent hypotension should warrant search for other causes, such as sepsis myocardial
infarction and pulmonary thromboembolism or use of narcotics or positive pressure ventilation"
Gastrointestinal motility disorders occur in *,I of severely a'ected GBS patients" 7leus is associated with
other features of dysautonomia (tachycardia and hypertension)" (ysmotility can be e'ectively managed by
suspension of enteral feeds, nasogastric suctioning, and erythromycin or neostigmine"
4yponatremia is the common electrolyte abnormality in GBS and is due to S7#(A (in ma3ority of the
cases) and natriuresis" %he treatment is di'erent for both" Both re>uire replenishment of sodium but S7#(A
need !uid restriction and in case of natriuresis re>uires intravascular volume epansion" %he best way to
di'erentiate these two conditions is by measuring central venous pressure"
P*&sical T*"%a)&
%he goals of the therapy programs are to reduce functional de0cits and to target impairments and
disabilities resulting from GBS" 5arly in the acute phase of GBS, patients may not be able to fully
participate in an active therapy program" #t that stage, patients bene0t from daily 6;4 eercises and
proper positioning to prevent muscle shortening and 3oint contractures" #ddressing upright tolerance and
endurance also may be a signi0cant issue during the early part of rehabilitation"
#ctive muscle strengthening can then be slowly introduced and may include isometric, isotonic,
isokinetic, or progressive resistive eercises" 4obility skills, such as bed mobility, transfers, and
ambulation, are targeted functions" 2atients should be monitored for hemodynamic instability and cardiac
arrhythmias, especially upon initiation of the rehabilitation program" %he intensity of the eercise program
also should be monitored, because overworking the muscles may, paradoically, lead to increased
%his treatment also known as plasma echange is a type of RbloodcleansingR in which damaging
antibodies are removed from your blood" 2lasmapheresis consists of removing the li>uid portion of your
blood (plasma) and separating it from the actual blood cells" %he blood cells are then put back into your
body, which manufactures more plasma to make up for what was removed" 7tSs not clear why this
treatment works, but scientists believe that plasmapheresis rids plasma of certain antibodies that
contribute to the immune system attack on the peripheral nerves"
2lasma echange was the 0rst treatment that was found to be e'ective in hastening recovery in
patients with the GuillainBarr syndrome, and it appeared to be most e'ective when it was started within
the 0rst @ weeks after disease onset in patients who were unable to walk" 2lasma echange nonspeci0cally
removes antibodies and complement and appears to be associated with reduced nerve damage and faster
clinical improvement, as compared with supportive therapy alone" %he usual empirical regimen is 0ve
echanges over a period of @ weeks, with a total echange of , plasma volumes" ;ne trial showed that
patients who could walk with or without aid but could not run bene0ted from two echanges of *", plasma
volumes, but more severely a'ected patients re>uired at least four echanges"
Intravenous Immunoglobulin
%reatment with intravenous immune globulin, initiated within @ weeks after disease onset, is
reported to be about as e'ective as plasma echange in patients with the GuillainBarr syndrome who
cannot walk independently" 7t is thought that immune globulin may act by neutraliBing pathogenic
antibodies and inhibiting autoantibody.mediated complement activation, resulting in reduced nerve in3ury
and faster clinical improvement, as compared with no treatment,CC,C+ although no comparative studies
have been performed" 7n general, intravenous immune globulin has replaced plasma echange as the
treatment of choice in many medical centers because of its greater convenience and availability" #ccording
to the standard treatment regimen, immune globulin is given at a total dose of @ g per kilogram of body
weight over a period of , days"
#lthough some people can take months and even years to recover, most cases of Guillain.Barre
syndrome follow this general timelineK
$ollowing the 0rst symptoms, the condition tends to progressively worsen for about two weeks"
Symptoms reach a plateau and remain steady for two to four weeks"
6ecovery begins, usually lasting si to *@ months"
%his syndrome is fatal in P @I" 4ost patients improve considerably over a period of months, but
about GEI of adults and even more children have some residual weaknessat G yr" 2atients with residual
defects may re>uire retraining, orthopedic appliances, or surgery

#fter initial improvement, G to *EI of patients develop chronic in!ammatorydemyelinating
polyneuropathy (&7(2Tsee below)"6ecovery can take weeks or years" 4ost people survive and recover
completely" #ccording to the 1ational 7nstitute of 1eurological (isorders and Stroke, about GEI of patients
still have some weakness after G years" 4ild weakness may persist for some people" # patientSs outcome is
most likely to be very good when the symptoms go away within G weeks after they 0rst started
5ia&nosis5 In"7"cti1" B%"at*in( Patt"%n %"lat"' to %a)i'l& )%o(%"ssin( %"s)i%ato%& $!scl"
*" 4onitor respiratory status through vital capacity measurements, rate and depth of respirations, and
breath sounds"
@" 4onitor level of muscle weakness as it ascends toward respiratory muscles" :atch for
breathlessness while talking which is a sign of respiratory fatigue"
G" 4onitor the patient for signs of impending respiratory failure"
H" 4onitor gag re!e and swallowing ability"
," 2osition patient with the head of bed elevated to provide for maimum chest ecursion"
D" (etermine the parameters for mechanical ventilation(vital capacity of less than *, ml<kg,partial
pressure of oygen less than CEmmhg and progressive bulbar weakness"7f re>uired mechanical
ventilation is initiated"
C" Suctioning is needed to maintain a clear airway"
+" %each patient about breathing eercises or use of an incentive spirometer to reestablish normal
breathing patterns"
5ia&nosis* I$)ai%"' )*&sical $o/ilit& %"lat"' to )a%al&sis
*" #ssess the level of physical mobility of the patient"
@" %he paralyBed etremities are supported and range of motion eercises are initiated
G" 1ursing interventions are aimed at preventing (=%
H" 6ange of motion eercises, position changes, anticoagulation, use of thigh high elastic stockings
and ade>uate hydration is needed to prevent complications of (=%
," 2adding should be placed over the bony prominences such as elbows and heels to prevent bed
D" 2osition the patient from side to side every @ hours to prevent the risk of developing decubitus
C" 2rovide regular skin care to include pressure area management"
5ia&nosis5 I$/alanc"' n!t%ition5 l"ss t*an /o'& %"9!i%"$"nt %"lat"' to ina/ilit& to s8allo8
,. #ssess the nutritional re>uirement of the client.
-. #ssess for the presence of paralytic ileus,if present initiate 7= !uids and parenteral feedings should
be initiated" 4onitor for return of bowel sounds"
.. 7f the patient cannot swallow due to bulbar paralysis, gastrostomy tube is placed to supply
/. #ssess the gag re!e and bowel sounds before administering nutrients"
5ia&nosis* Hi(* %is4 o% i$)ai%"' s4in int"(%it& %"lat"' to i$$o/ilit& as "1i'"nc"' /& asc"n'in(
,. &hange patient position every @ hours"
-. 6emove wet<wrinkles linens promptly"
.. (evelop a repositioning schedule for client, involving client in reasons for and decisions about
times and positions in con3unction with other activities"
/. 5levate both legs with pillow"