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What are the 2 types of complex regional pain syndrome (CRPS)?
type 1: reflex sympathetic dystrophy
type 2: causalgia
Describe type 1 CRPS
develops after noxious event (crush or soft tissue injury, immobilization, surgery)
spontaneous pain or hyperalgesia/allodynia
edema, vascular abnormalities
abnormal sudomotor activity
non-nerve origin
Describe type 2 CRPS
develops after nerve injury
not limited to territory of injured nerve
edema, skin blood flow abnormality
abnormal sudomotor activity
What are the clinical features of CRPS?
pain
marked Sx’s more distally
progress in intensity and spread proximally
What structural impairments are caused by CRPS?
motor dysfunction (weakness, tremor, dystonia)
edema or sweating asymmetry (hypo or hyperhidrosis)
vasomotor instability (temperature or skin color asymmetry)
trophic ∆s (increase/decrease hair & nail growth, or skin ∆s)
What functional impairments are caused by CRPS?
pain avoidance behaviors → mm atrophy or osteopenia/osteoporosis
slower at initiating movements
abnormal gait
Describe Paget disease (osteitis deformans)
osteometabolic disorder characterized by accelerated skeletal remodeling that produces a slowly progressive enlargement & deformity of multiple bones
asymptomatic or gradual Sx’s
phase I (osteolytic phase): bone resorption & hypervascularization
phase II (sclerotic phase): reflecting previously increased bone formation but currently decreased cellular activity & vascularity
phase IIL (mixed phase): both active bone resorption & compensatory bone formation → disorganized skeletal architecture (bones become sponge-like, weakened, deformed)
What are the complications of Paget disease?
fx
delayed union
chronic bone pain (achy, worse at night, better w/ activity)
facial or ocular nerve compression
spinal stenosis or myelopathy
pagetic arthritis
How is Paget disease treated?
meds or surgery
Describe tethered spinal cord
fixation of the spinal cord in an abnormal caudal location d/t adhesions at the site of the original back lesion
the child is growing rapidly but the cord is not free to slide up & reposition as it should
excessive stretch to the spinal cord → metabolic ∆s & ischemia of the neural tissue → degeneration in mm function
What are the clinical features of tethered spinal cord?
spasticity of mms w/ sacral nerve roots
increased lumbar lordosis
back or buttock pain
scoliosis at a young age that rapidly progresses
scoliosis above the level of paralysis
bowel & bladder ∆s
gait ∆s
LE weakness & atrophy
What are the Ottawa ankle rules?
Ankle X-ray if any of the following:
bone tenderness at posterior edge of distal 6cm or tip of lateral malleolus
bone tenderness at posterior edge of distal 6cm or tip of medial malleolus
inability to WB 4 steps immediately after injury or in the ED
Foot X-ray if any of the following:
bone tenderness at the navicular bone
bone tenderness at the base of the 5th metatarsal
What are the Canadian C-spine rules?
Any of these high risk factors? If yes → X-ray
age ≥65 years
dangerous MOI
paresthesias in extremities
If none, any of these low risk factors? If none of these → X-ray
simple rear-end MVA
sitting in the ED
ambulatory at any time
delayed onset of neck pain
no midline C-spine tenderness
If one of the above, able to rotate neck 45° on both sides? If unable to → X-ray
If yes → no X-ray
Describe upper UTI & their Sx’s
inflammation or infection of the kidney or ureters (pyelonephritis, glomerulonephritis)
unilateral costovertebral tenderness
flank pain
ipsilateral shoulder pain
Describe lower UTI & their Sx’s
inflammation or infection of the bladder or urethra (cystitis, urethritis)
urinary urgency
pain in low back, abdomen, pelvis
dysuria (pain w/ urination)
What is primary prevention?
disease prevention
What is secondary prevention?
early detection & treatment in asymptomatic pts → reduce severity or duration of disease → improve outcomes
What is tertiary prevention?
reduce disease impact and manage Sx’s in diagnosed pts through rehab & management of existing conditions to prevent complications