L10 Guillain Barre

Question 1

GBS: basic definition

Answer 1

immune mediated polyneuropathy from preceding infection reacting with AND and causing nerve root inflammation

Question 2

GBS causes what kind of neuropath(y/ies)?

Answer 2

motor and sensory paralytic neuropathy

Question 3

3 rare types of GB

Answer 3

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

Question 4

epidemiology/risk factors of GB

Answer 4

1-2/100k
increases 20% risk every 10 years of life
more in older ages, men>women, still possible in children

Question 5

GB pathophys

Answer 5

cell mediated PN disruption mediated by immune cells responding to infection
secondary hypersensitivity reaction occurs involving elevated cytokines in CSF, PN, and serum

Question 6

basic pathogenesis of GB

Answer 6

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

Question 7

GB subtypes

Answer 7

acute inflammatory demyelinating polyneuropathy - demyelination of nerve root from antibodies
acute motor axonal neuropathy - axon and myelin affected, creating more damage from antibodies

Question 8

cells activated in GB

Answer 8

macrophages and T lymphocytes
complement system
antibodies

Question 9

effects of myelin destruction on individual neurons

Answer 9

disrupted conduction with myelin and axon destruction

Question 10

chronic inflammatory demyelinating polyneuropathy

Answer 10

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

Question 11

GBS clinical presentation

Answer 11

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

Question 12

GBS s/s

Answer 12

N/T
ascending muscle weakness distal to proximal
areflexia
hypotonia
autonomic: tachycardia, low CO, arrhythmia, hypo/hypertension peripheral blood pooling, urinary retention

Question 13

what type of sensory loss in common in GBS?

Answer 13

myelinated senses
proprioception, vibration, discriminative touch
N/T, paresthesia
increase in pain/muscle aching
hypersensitivity/burning

Question 14

functional loss in GBS

Answer 14

mobility/gait
transfers
standing
seated postural stability
fatigue
orthostasis

Question 15

clinical progression of GBS

Answer 15

progresses over 2-4 weeks, 90% stop progressing by then
weakness ascending, may lead to ventilation which has a poorer prognosis

Question 16

does CIDP of GBS have a slower onset?

Answer 16

CIDP, 8 weeks vs 2-4

Question 17

duration of CIDP treatment vs GBS

Answer 17

sustained treament for CIDP, GBS only needs treatment until symptoms stabilize

Question 18

assessments for clinical diagnosis of GBS

Answer 18

progressive weakness in one of more limbs
symmetrical N/T
decreased DTRs
no fever
CN involvement: dysphagia, V, VII, IX, X, XI, XII

Question 19

diagnostic testing for GBS

Answer 19

lumbar puncture - leukocytes decreased and CSF fluid proteins elevated
Nerve conduction velocity abnormal

Question 20

spinal tap is conducted by:

Answer 20

needle injection below L1/L2 where spinal cord ends and cauda equina begins
patient is in curled up position to flex spine

Question 21

three phases of GBS

Answer 21

initial: 1-3 weeks, definitive symptoms
plateau: days-2 weeks
recovery: 4-6 months to 2 years (years if nerve damage)

Question 22

plasmapheresis

Answer 22

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

Question 23

IVIg

Answer 23

intravenous administration of immunoglobulins
inhibits autoantibodies to reduce or block secondary immune attack and reduce phagocytic damage
as effective but must be implemented immediately

Question 24

nadir

Answer 24

point in GBS where disease stops progressing/ascending

Question 25

medical prognosis in GBS

Answer 25

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

Question 26

negative prognostic signs in GBS

Answer 26

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

Question 27

long term outcomes of GBS

Answer 27

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

Question 28

systems review for GBS

Answer 28

cognition integumentary: very susceptible to ulcers, loss of sensation needs to be assessed to measure progression

Question 29

considerations for GBS

Answer 29

skin integrity DVT: risk due to lack of movement and long hospital stay autonomic dysfunction aspiration: dysphagia

Question 30

PT assessment of GBS

Answer 30

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

Question 31

ICU care management for GBS pt

Answer 31

family training ROM/positioning supported upright sitting with close monitoring, 10-20 min and BP checks prevent contractures and skin breakdown

Question 32

goals of GBS pt in ICU

Answer 32

prevent contractures: ROM and resting splints, positioning, AFO, exercise promote mobility OOB: once nadir achieved; manage OH, work up to WB with tilt table

Question 33

positioning for GBS

Answer 33

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

Question 34

acute care goals for GBS pts

Answer 34

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

Question 35

goals for GBS pts in rehab

Answer 35

tolerate 3 hours per day of rehab dysphagia management strengthening function: gait, transfers, endurance, postural control

Question 36

precautions to exercise in the acute phase

Answer 36

avoid fatigue and don't push patient as they will collapse! muscle weakness, orthostasis, lack of equilibrium, lack of protective responses increase fall risk

Question 37

type of orthotic to prevent GBS pts from collapsing while walking

Answer 37

AFO w anterior support to prevent knee collapse