L10 Guillain Barre Flashcards
GBS: basic definition
immune mediated polyneuropathy from preceding infection reacting with AND and causing nerve root inflammation
GBS causes what kind of neuropath(y/ies)?
motor and sensory paralytic neuropathy
3 rare types of GB
acute motor axonal neuropathy: axons damaged instead of myelin, arm and leg involvement
acute motor sensory axonal neuropathy: combo of myelin and axon damage
miller fischer syndrome: rare variant with weakness or paralysis of the eye muscles
epidemiology/risk factors of GB
1-2/100k
increases 20% risk every 10 years of life
more in older ages, men>women, still possible in children
GB pathophys
cell mediated PN disruption mediated by immune cells responding to infection
secondary hypersensitivity reaction occurs involving elevated cytokines in CSF, PN, and serum
basic pathogenesis of GB
2/3rds associated with bacterial or viral infection ~2 weeks before, GI or respiratory
includes campylobacter, cytomegalovirus, epstein barr, HIV
can also be caused by another event like surgery or immunization, trauma, bone marrow transplant
GB subtypes
acute inflammatory demyelinating polyneuropathy - demyelination of nerve root from antibodies
acute motor axonal neuropathy - axon and myelin affected, creating more damage from antibodies
cells activated in GB
macrophages and T lymphocytes
complement system
antibodies
effects of myelin destruction on individual neurons
disrupted conduction with myelin and axon destruction
chronic inflammatory demyelinating polyneuropathy
subset of guillain barre with a slow progression over 8 weeks
CIDP doesn’t involve respiratory
rarely comes from infection
relapses more frequently with longer recovery time
treated w corticosteroids
GBS clinical presentation
acute presentation ascending over 3-4 weeks
symmetrical ascending weakness from distal LE to UE/respiratory system
severe fatigue
may be intubated from respiratory muscle weakness
GBS s/s
N/T
ascending muscle weakness distal to proximal
areflexia
hypotonia
autonomic: tachycardia, low CO, arrhythmia, hypo/hypertension peripheral blood pooling, urinary retention
what type of sensory loss in common in GBS?
myelinated senses
proprioception, vibration, discriminative touch
N/T, paresthesia
increase in pain/muscle aching
hypersensitivity/burning
functional loss in GBS
mobility/gait
transfers
standing
seated postural stability
fatigue
orthostasis
clinical progression of GBS
progresses over 2-4 weeks, 90% stop progressing by then
weakness ascending, may lead to ventilation which has a poorer prognosis
does CIDP of GBS have a slower onset?
CIDP, 8 weeks vs 2-4
duration of CIDP treatment vs GBS
sustained treament for CIDP, GBS only needs treatment until symptoms stabilize
assessments for clinical diagnosis of GBS
progressive weakness in one of more limbs
symmetrical N/T
decreased DTRs
no fever
CN involvement: dysphagia, V, VII, IX, X, XI, XII
diagnostic testing for GBS
lumbar puncture - leukocytes decreased and CSF fluid proteins elevated
Nerve conduction velocity abnormal
spinal tap is conducted by:
needle injection below L1/L2 where spinal cord ends and cauda equina begins
patient is in curled up position to flex spine
three phases of GBS
initial: 1-3 weeks, definitive symptoms
plateau: days-2 weeks
recovery: 4-6 months to 2 years (years if nerve damage)
plasmapheresis
first treatment option for GBS
plasma exchange done by removing blood from plasma, centrifugal separation to remove immune cells/antibodies and reinject into patients
must be started within 2 weeks
IVIg
intravenous administration of immunoglobulins
inhibits autoantibodies to reduce or block secondary immune attack and reduce phagocytic damage
as effective but must be implemented immediately
nadir
point in GBS where disease stops progressing/ascending
medical prognosis in GBS
50% andir by 1 week, 70% 2, 80% 3
3-5% die from organ failure/respiratory
recovery starts in 2-4 weeks with fatigue and endurance as long term consequences
negative prognostic signs in GBS
older age 40+
rapid rate of progression <7 days
longer length of time to nadir
severe muscle weakness
CN involvement w loss of eye movement or dysphagia
needing ventilation
distal motor response amplitude reduces to less than 20% of normal
preceding diarrheal illness or cytomegalovirus
long term outcomes of GBS
independent ambulation: 80% achieve at 6 months
full strength recovery: 60% achieve at one year
5-10% are vent dependent for months
5% die
20% on vents die
relapse: 10%
2% develop CIDP
systems review for GBS
cognition
integumentary: very susceptible to ulcers, loss of sensation needs to be assessed to measure progression
considerations for GBS
skin integrity
DVT: risk due to lack of movement and long hospital stay
autonomic dysfunction
aspiration: dysphagia
PT assessment of GBS
neuromuscular: reflexes, tone,e tc
muscular: ROM, strength, PROM
cardiopulmonary: cough, inhale/exhale, diaphragm
CV: BP in supine, seated, standing
CN
Pain: neuro/PROM or muscular/AROM
transfers
gait
precautions for autonomic changes, DVT, aspiration
ICU care management for GBS pt
family training
ROM/positioning
supported upright sitting with close monitoring, 10-20 min and BP checks
prevent contractures and skin breakdown
goals of GBS pt in ICU
prevent contractures: ROM and resting splints, positioning, AFO, exercise
promote mobility OOB: once nadir achieved; manage OH, work up to WB with tilt table
positioning for GBS
protect heels by “floating” at end of bed
supine: pillow between legs
sidelying with arm and wrist supported/straight
alternate supine/sidelying every 2 hours
acute care goals for GBS pts
upright chair sitting 2-3 hours a day
initiate transfer and bed mobility training
promote graded activity
initiate WB activity w AD/orthotics
avoid prolonged positioning
goals for GBS pts in rehab
tolerate 3 hours per day of rehab
dysphagia management
strengthening
function: gait, transfers, endurance, postural control
precautions to exercise in the acute phase
avoid fatigue and don’t push patient as they will collapse!
muscle weakness, orthostasis, lack of equilibrium, lack of protective responses increase fall risk
type of orthotic to prevent GBS pts from collapsing while walking
AFO w anterior support to prevent knee collapse
