Test 2: Special Considerations and Differential Flashcards
describe the filling phase associated with normal micturition
voluntary control over LUT ivolved complex interactions between ANS and SNS (pudendal nn) efferent pathways
empty bladder = sympathetic efferents from T11-L2 inhibit contraction of bladder wall (detrusor) and maintain contraction of internal sphincter
bladder fills = proprioceptors sense stretch = sends impulse to SC S2-S4
spinal cord relays signals:
- up cord to brain to signal fullness
- reflexive signal stimulates Sympathetic and parasympathetic branches to initiate emptying
describe the capacity of the bladder in the filling phase
neuro or anatomical compromise = store quantity of 200-300 ml before signal is emitted from stretch receptors
max capacity = 500ml for females and 700 ml for males
overwhelming urge occurs at ~90% capacity (2 cups for females, 20 oz for males)
describe the normal emptying phase
conditions met = frontal lobe disinhibits PMC = pontine micturition center = parasymathetic activation = detrusor contraction + relaxation of IUS
conditions not met = frontal lobe inhibits PMC = pelvic floor mm contract to keep EUS closed
as signals from pontine micturition center relax the IUS, PMC also signals SC to inhibit pelvic floor mm
describe normal defecatory function
similar to the bladder
rectum has very sensitive stretch receptors that send signal to cord when the rectal cavity is full
rectum is full = signal to SC and splits with signal to brain
decision from cortex results in:
1. delay of urge through contraction of pelvic floor and EAS
2. no response from cortex = reflexive defecation
describe LMN role in normal bowel reflexive evacuation
normal bowel reflexive evac involves LMN from SC transmitting signals to cord of rectal distention
parasympathetic response = increase GI activity
sympathetic response = decrease GI activity
describe bladder development
begins at 4-6 weeks gestation
in infants and kids, urinary bladder is in the abdomen even when empty and enters the greater pelvis by 6 years of age but is not located entirely in the lesser pelvis until after puberty
intermittent vs continuous urinary incontinence in children
intermittent = at least 5 years of age with either episodes of day or night wetting
continuous = as name indicates with the implication of either an anatomical and/or neuro deficit
incidence of incontinence in kids
high
15.5% rate for enuresis in 7.5 year old kids
decreases with age but remained at 0.5-1% in adults
given close nature of GU and rectum/GI systems, children should be assessed for constipation through care for LUT dysfunction
how long is micturition involuntary in kids
3-5 years
volitional control can occur as early as 1 year
hypothesis that high absorbance diapers leads to later incontinence
what is nocturnal enuresis
bedwetting
genetic component
> 5 years of age
males at higher risk
other risk factors: neuropsychiatric disorders (ADD/ADHD), intellectual disorders, sleep disorders
pediatric pelvic floor intervention examples
timed/schedule voiding
habit training
- limit fluid intake before bed
- pee before bed
- parent wakes child w/i 1st segment of night to trigger arousability
External pelvic floor exam (parent present + consent)
biofeedback training (external sensors)
NMES (external sensors for PFM coordination and strengthening)
pelvic girdle mm training
etiology of tethered cord syndrome
vertebral column grows longer than the spinal cord
infrequent = SC attached to surrounding structures during early development
as column elongates, tethered cord becomes stretched and damages SC/causes cauda equina
red flag if symptoms have not be previously diagnosed/addressed
causes of tethered cord syndrome
scar tissue
fatty mass/lipoma
abnormal development
S&S of tethered cord
LBP! and LE pain
difficulty walking
excessive lordosis/scoliosis
problems with bowel/bladder control
change in LE strength
foot deformities
LMN S&S if cauda equina
UMN S&S if SC affected
abnormal integument signs (dimple, tuft of hair, hemangioma, bulge of fatty mass)
sx indicated if severe
what is an overactive bladder (OAB)
includes decreases in bladder capacity, urethral compliance, maximal urethra closure pressure, and urinary flow rate
often occurs from “urinating just in case”
can lead to urge incontinence
factors that increase likelihood of incontinence with aging (especially females)
anatomy, decrease in periurethral blood flow due to lack or decreased estrogen
what happens with urinary incontinence in both men and women
postvoid residual volume and the prevalence of involuntary detrusor mm contraction likely increase while urethral resistance increases in men
prevalence of UI and the 2 types
more than 50% nursing home residents
established = usually result of neuro damage, intrinsic bladder or urethral pathology
transient = UI caused by changes in meds, diet, hygiene (typically reversible if underlying problem is addressed)
transient causes of UI (DIAPPERS)
Delirium
Infection (especially UTI)
Genitourinary Syndrome of Menopause (atrophic vaginitis)
Pharmaceuticals
Psychological Factors
Excess fluid output (i.e. dietetics)
Restricted mobility
Stool (constipation or impaction)
types of urinary incontinence
stress = unopposed increases in intraabdominal pressure
urge = sudden urge to urinate without ability to hold in urine once urge sensation occurs
mixed = combo of UUI and SUI
overflow = accidental loss of urine from chronically full bladder
functional = inability to get to bathroom bc of physical limits or inability to manage clothing once individual has made it to bathroom
what may cause overflow incontinence
may result due to physical alignment issues or damage to bladder nn from diabetes
loss of adequate estrogen or progesterone
herniated L/S disc
may also be due to detrusor instability; varable volume emptied but not completely emptied
what does traditional PFT consist of
uptraining/progressive resistance exercise (PRE)
- independent or in conjuction with biofeedback, NMES
downtraining/relaxation
- independent or in conjunction with biofeedback
pelvic floor intervention examples for adults
general mobility = gait, bed mobility, transfers, finger dexterity, strengthening
bladder/bowel logs = apply strategies based on how/when oncontinence occurs
“Knack” training = timing/coordination of pelvic floor contraction with exhale to counteract increases in intraabdominal pressure
scheduling
- fluid restriction before bed
- pee before bed
- time intervals for urination (2-3 hrs in SNF)
edu on bladder irritants
- may cause pain or increase frequency
- acidic, spicy, caffeinated, carbonated, chocolate, concentrated urine
traditional pelvic floor therapy
causes of fecal incontinence
psychological (depression, anxiety, disoriented, etc)
neuro impairments (sensory/motor due to CVA, diabetes, PD, autonomic neuropathy, etc)
anal sphincter dysfunction (risk factor = 4th degree tear with labor)
hemorrhoids, rectal prolapse, or rectocele
severe diarrhea (infection, severe impaction, etc); long standing constipation = cant sense stool movement and stretch receptors are no longer stimulated
interventions for fecal incontinence
team effort for why S&S are occuring
- diet
- med changes
- function changes
- voiding programs
- recs on fiber/H2O consumption
PFPT
- biofeedback helpful in 70% people due to sensory/motor probs; rectal balloon training for over dilated rectum (attempt to regain compliance)
- NMES
2 types of neurogenic bladder
- LMN alterations from T12 and below have flaccid bladder and sphincters/unable to store urine = “autonomous neurogenic bladder”
- UMN defects; failure to empty = “reflexive neurogenic bladder”
describe what happens with an UMN reflexive neurogenic bladder
defects from T12-L1 = generally reflexive bladder which may be hyperreflexive or hypertonic
brain doesnt recieve signal that bladder is full and signal to delay urge to urinate is not transmitted
hyperreflexive bladder reflex
- spontaneous bladder emptying with occasional residual due to detrusor sphincter dyssynergia
- initiating voiding is problematic due to lack of coordination between bladder contraction and sphincter relaxation
describe a suprapubic catheter
implanted through lower abdominal wall
PT should be aware of gait belt placement/disruption of covering
may be placed for better pt management but often it is due to a wound in perineal/buttock region to keep moisture away from site
describe intermittent catheterization
used when unable to initiate urination or in times of incomplete emptying
acute care and IPR - initiated by nursing
inpatient and outpatient - pt should bring their cath kit; therapist assesses for AD
describe indwelling catheters
typically used early in recovery
kinked or at capacity - may contribute to AD
describe a condom catheter
option for males
can be an option for episodes of incontinence in UMN but can also be used as long term strategy for those with LMN injuries
typically used with leg bad
can slip off if ill fitting!
may or may not get dirupted during seating and mobility
describe use of adult briefs
usually last resort
can be used alone or in conjunction with other methods
risk for skin breakdowns/excessive moisture or yeast/bacterial infections in females
interventions for neurogenic bladder
ask about schedule/management methods
early rehab = train with nursing
lifespan = consider how pt functions in seating system; materials, wicking system, risk of AD, etc
if pt has difficylty initiating = edu on tapping strategies
incomplete SCI may or may not respons to traditional motor interventions
- biofeedback
- NMES
- traditional strengthening of PFM
describe management of UMN neurogenic bowel with SCI pts
reflexive bowel emptying occurs when reflex is triggered
- depends on fullness of colon
- can be triggered by food, movement of feces, or suppository/stimulation
- UMN = T12-L1 and above
continence dependent on triggering reflexes and complete bowel evac
parasympathetic innervation creates sphincter tone and reduces changes of FI
describe management of LMN areflexive bowel with SCI pts
LMN lesion interferes with reflexive evac
- loss of motor tone and flaccidity
- peristalsis may be slowed with water reabsorption and this can increase risk of constipation that leads to impaction and AD
- rectal sphincter may fail to contain stool = incontinence
LMN lesions = below T12-L1
continence depends on keeping rectal cavity empty and doing a full evac
Special considerations for multiple sclerosis in regard to bowel/bladder
CNS lesions between pons and sacral nn = increased urge, frequency, urge incontinence, voicing dysfunction, and urinary retention
demyelinating CNS lesions = slow colon transit and decrease rectal sensation/contractile response
meds can lead to constipation/fecal incontinence
B&B impairments are most common problems that limit those with MS; QOL, social life, and finances
PD special considersations B&B
pelvic autonomic dysfunction doesn’t respond well to levodopa like motor symptoms do
B&B S&S have strongest correlation with QOL
UI and constipation arent always addressed with these pts
UPDRS has questions about bowel and bladder
S&S of cauda equina
LBP and sciatica; increases with abdominal pressure and decreases with lying down
decreased sensation
ANS S&S = retention or incontinence
motor = paresis or paralysis of nn roots involved
reflexes are diminished for impaired nn roots
prognosis for cauda equina
marked improvements with sx decompression
greater chance of persistent problems w/o sx
big picture/red flag for cauda equina
LBP and sciatica combined with NEW bowel and bladder retention or incontinence S&S requires emergency referral as it may progress to paraplegia and permanent ANS problems
deep gluteal syndrome pain pattern (aka piriformis syndrome)
piriformis attaches proximally at sacrum, sacrotuberous ligament, near PSIS to greater trochanter
may not just be piriformis onvolved (consider OI, SG, IG)
common site for sciatic nn compression
differential dx
- coccyx pain
- L/S radiculopathy/referred pain
- deep hip ER pathology
- pudendal neuralgia
deep gluteal syndrome is compression of what and what are the subtypes
sciatic or pudendal nn due to non-discogenic pelvic lesions
- piriformis syndrome
- gemelli-obturator internus syndrome
- ischiofemoral impingement syndrome
- proximal hamstring syndrome
symptoms of deep gluteal syndrome
deep buttock ache
pain with ant pelvic tilt in quadruped (proximal HS)
with or without neurologic symptoms
diagnostic tests for deep gluteal syndrome
pelvic MRI and or EMG depending on S&S
US guided injections (diagnostic and intervention)
what might deep gluteal syndrome co-occur with
bursitis (trochanteric or ischial)
pelvic floor referral patterns/possibilities
symptoms of bowel/bladder
pain in groin (“golf ball in rectum”)
saddle anesthesia (pudendal nn compression or something else)
piriformis syndrome - deep butt pain/dull ache
coccydynia - pain with sitting, or possibly with defecation
Prevalence of labral tears with hip pathology
prevalence of labral tears in pts with hip/groin pain = 22-55%
can cooccur with pelvic floor guarding/pain
may be related to childhood pathologies
postpartum women = increased risk of labral tears intrapartum and at delivery (ER during delivery is recommended to reduce risk; small study though)
S&S of femoroacetabular impingement
pain in hip FLX
clicking/popping with activity
stiffness
FADIR (not used in isolation; cluster)
explain the correlation between FAI and inguinal hernia
strong correlation
ROM limits from FAI may contribute to formation of hernia
bulge is present
replication of S&S or increased bulge with increased intra abdominal pressure
what is a stress fx
caused by repeated submax stress
better with rest; may be painful at rest with prolonged exposure/microfx
increases with activity
factors influencing include:
- training
- biomechanics
- bone health
- footwear
MRI is most comprehensive method to evaluate
for pelvic or sacral stress fx individuals may exhibit what
inguinal, perineal, pubic rami, and/or adductor region pain
sacral stress fx may elicit + FABER
what is RED-S and the implications
relative energy deficiency in sport
results from low energy diets and excessive exercise
term encompasses both male and female populations
energy reduction reduces release for gonadotropic releasing hormone (neg affect on bone health)
relative risk of stress fx in athletes with menstrual disturbances is 2-4x that of eumenorrheic athletes
what is dysuria
painful urination
what is hematuria
blood in urine
S&S that indicate the GU system
may have skin hypersensitivity (T10-L1)
pelvic or genital masses
abnormal discharge
genital pain
may or may not have fever
how do anticholinergics/antispasmodics work and what are the adverse side effects
i.e. oxybutynin (for overactive bladder)
may reduce spasm or smooth mm contraction
adverse effects = dizziness, drowsiness, blurred vision, dry mouth, increased HR
how do tricyclic antidepressants work and what are the adverse effects
i.e. amitriptyline
produces strong inhibitory effect on bladder smooth mm
adverse effects = weakness, fatigue, parkinsonian effect, postural hypotension, HA, irritability, abdominal stress
elderly = increase risk for side effects
what are alpha adrenergics
i.e. ephedrine, pseudoephedrine
increases bladder outlet resistance
adverse effects = tachycardia, cardiac arrhythmias, vertigo, HA
what are beta adrenergic blocks
i.e. propanolol
increases bladder outlet resistance
adverse effects = bradycardia, lightheadedness
how do estrogens work with bladder management
increases periurethral flow
strengthens periurethral tissues
adverse effects = HA, nausea, edema, HTN
medications to relax striated mm
baclofen (oral)
dantrolene sodium (skeletal mm relaxants)
diazepam (benzodiazepine)
relax external sphincter by inhibiting postsynaptic reflexes of strained mm
adverse effects = weakness/sedation
what is an intrathecal baclofen pump
intrathecal dosage instead of oral
less systemic side effects
