Polio Flashcards
Pathogenesis
highly contagious virus
oral route of transmission (oral-fecal)
replicates in lymphatic tissue of GI tract
spreads throughout body
asymptomatic primary transient viremia (minor)
3 patterns
asymptomatic- majority
non-paralytic infection- develop flu-like symptoms, small fraction develop CNS symptoms; stiff neck, fever, N&V, 4-8%
paralytic infection- .1% infected ppl
Spread of polio
possibly by crossing blood/brain barrier
possibly axonal transport from ms to SC to brain
leads to destruction of anterior horn cells and neurons in thalamus, brainstem, motor cortex
Clinical presentation
motor neurons in SC affected LMN in presentation 1-many muscles, tetraplegia, resp failure proximal>distal more affected LE>UE asymmetrical reflexes absent or decreased sensory normal
PT management
acute stage- ROM, positioning, pain relief; ms pain, cramps
rehab stage- strengthening what ms left, orthotics, functional mobility training (poor MMT but have adapted), decrease consequences
Prognosis
<10% die with modern tx
no way to predict recovery potential
regain strength in partially denervated ms up to year later
Vaccines
Salk vaccine- 2 IM injections of inactive virus at 1 month, booster at 6 mo, Now called IPV
Sabine vaccine- live virus given orally at 2,4, and 18 months, booster at 4-6 yo; now called OPV; cheaper
IPV preferred d/t slight rik of getting polio from live vaccine
1-2 does of booster if:
planning of traveling to foreign country with high polio
lab worker handles polio
health are worker who tx pts who have polio
if survive initial attack of polio should still be immunized
Post-polio syndrome Prevalence
300,000 polio survivors in US with paralytic form; of those, 1/4 to 1/2 have new health problems
S/S of PPS
fatigue and decreased endurance weakness in ms both affected from original polio and new ms and jt pain breathing difficulties intolerance to cold fasiculations symptoms appear to progress slowly
risk factors for PPS
age of original polio dx (older more likely)
extent of initial recovery (better recovery more likely)
Dx of PPS
prior episode of Polio
hx of >15 yrs stable neuro function
gradual onset of symptoms
exclusion of other conditions causing similar symptoms
Etiology of PPS
compensatory mechanism (motor unit enlargement) is overwhelmed; working motor neurons innervate ms fibers of wiped out ant horn cells and get overwhelmed
greater metabolic demand leads to failure of neurons transmission
effects of aging (loss of motor units)
Primary Functional Limitations PPS
inability to: climb stairs, perform WC transfers, dress I, walk
Energy conservation
prioritize activities of day so can do what you need to first