Test 3: AIDP Flashcards
what neuro conditions have we learned thus far that are LMN or PNS
SCI below L2
vestibular hypofunctions
AIDP
CIDP
post-polio
polyneuropathies
incidence of AIDP
100000 cases/year world wide
1-2 new cases per 100000 people
peak frequency of age is young adults or people in 5th to 8th decades
men more than women
white people
3-7% mortality rate
20% have lasting deficits
etiology of AIDP
common post campylobacter jejuni bacterial infection (most common cause for subtypes that involve axonal damage)
common after influenza, epstein barr, cytomegalovirus
also common after vaccines and sx
90% of pts who got GBS had viral or bacterial infection in the 30 days prior
pathophysiology of AIDP
peripheral nerves
can attack sensory and motor
AIDP = min sensory
anti-inflammaotry process involving T cells and macrophages resulting in demyelination
particularly affects nodes of ranvier
can have damage all the way to axons
S&S of AIDP
B ascending weakness
rapid and progressive initially
absence of DTRs
AMAN: acute motor axonal neuropathy
more severe
more likely to have respiratory involvement and vent dependence
significant residual S&S
ASAN: acute sensory ascending neuropathy
sensory changes more prominent than weakness
AMSAN: acute motor and sensory axonal neuropathy
ANS dysfunction is worse
may have:
- postural hypotension
- impaired sweating
- B&B changes
CIDP: chronic inflammatory demyelinating polyneuropathy
slower onset
may have relapses and remissions or progressive course over a year
describe the progressive phase of AIDP
ascending demyelination that progresses anywhere from 2-6 weeks
4 weeks avg impairment
can ascend to cranial nn and cause facial weakness
can involve resp. mm (30% need vent)
50% progressive phase ends at 2 weeks; 90% at 4 weeks
can also attack ANS
usually in acute care to be ready in case they need mechanical vent
plateau phase of AIDP
around 4 weeks when progression stops but remyelination has not fully occured
usually lasts 2-4 weeks
recovery phase of AIDP
nn start remyelinating and repairing
process takes months to years depending on level of damage
recovery happens proximal to distal
clinical diagnostic features of AIDP
B weakness and falccidity
decreased/absent DTRs
absence of alternative dx
additional features:
- mild sensory
- progress after 2-4 weeks
- CN involvement
- autonomic dysfunction
- absence of fever
CSF findings with AIDP
increased proteins after 1 week; increase continually with retest
less than 10 leukocytes/mm
nn conduction velocity testing findings with AIDP
slowest at 2 weeks
decreased across entire nn
fibrillation potential present in case of axonal damage
acute phase medical management for AIDP
admit them
monitor changes
be prepared to intubate if needed
2 main treatments of AIDP
high dose IVIG
plasmapheresis
dont have to do both
describe IVIG treatment
IG treatment
protein attacks foreign mechanism
need high dose
5 day course via IV
best for non-ambulatory adults in 1st 2 weeks of onset
describe plasmapheresis treatment
plasma exchange
filter blood plasma and remove antibodies
most effective w/i 2 weeks onset
pleateau phase med management
wean off vent
get into therapies
recovery phase medical management
track nn conduction recovery over time
refer to PT
indicators of a worse prognosis
age >40
delay in diagnosis
delay in treatment
C-jejuni infection cause
if vented at any point
better prognosis indicators
younger
no diarrhea preceding dx
lower level of disability S&S and admission
longer interval between onset and admission
no need for mechanical vent
recovery with AIDP
most recover in 1st year
still see changes up to 3 years
about 20% do not reach full recovery (may have residual neuropathic pain, autonomic changes, and distal weakness)
