PTRS 746
1. Osteoarthritis
Etiology-primary is idiopathic
Secondary- Increased age not “normal aging”, trauma- or repetitive microtrauma, obesity, infection
Pathophysiology-progressive destruction of articular cartilage due to loss of water and proteoglygans which causes loss of compressive stiffness and elasticity, bone forms in joint margins, *localized and confined to affected joints b. radiographic
Joint space narrowing, osteophytes and deformity
S/Sx-unequal joint involvement, lack of general symptoms, morning stiffness and after inactivity-but shorter duration than with RA, Pain is variable and worsens or occurs w/motion,
Joint distribution-DIPs, PIPs, thumb CMC, C-spine, L-spine, hips, knees, and 1 st MTP
Bouchard’s and Heberden’s nodes-osteophytes at PIP and DIP
Hips-protective position is flexion, abduction and ER,
Knee-protective position is flexion c. pharmacologic interventions.
Pharmacological-pain relief, but will not affect the disease progression, acetaminophen),
NSAIDs, corticosteroid injections, visco-supplementation w/hyaluronic injections,
Surgical intervention if pain, loss of function or progression of deformity. o Synovectomy-remove synovial membrane, soft tissue release, tendon transfer, o osteotomy-cut through the bone, o arthroplasty or arthrodesis-surgical fusion/immobilization of the joint d. PT plan of care
Subjective-pt hx, location of pain, duration, intensity, activity level, and fatigue, goals and red flags
Goals-decrease pain, increase/maintain functional joint ROM and strength, increase joint mobility and decrease stresses, increase functional endurance, max indep in ADLs, improve gait efficacy and safety, est exercise/conditioning program and educate family and pt on capacity for self management
PT plan-Acute-decrease pain/inflammation, rest joints, pain relief modalities (superficial heathot pack, deep heat-not acute, cold-acute, TENS) , maintain ROM, strength, endurance and functional independence training
Sub-acute-increase ROM, strength (isometrics at sub-max effort, dynamic conc/ecc in pain free range and incorporate functional activity, monitor inflammation=quads especially) and functional endurance training (non-WBing), increase range of ADLs and joint protectionposition/self ROM pay attention to positioning, goal is to lengthen/shorten muscles, exercise induced pain should subside in 1 hour, Manual therapy for OA, orthoses may be needed to maintain gained ROM, and reduce pain w/ambulation
Gait training-appropriate assistive device for walking speed and normalizing gait, cane can unload hip by 60%
Chronic-indep in ADLs, return to work, pt education
2. Rheumatoid arthritis
Pathophysiology-systematic inflammatory disease of the synovium with flareups, neutrophil infiltration, pannus-synovial (granulation)overgrow, invades/dissolves adjacent cartilage and bone w/fibroblasts and macrophages, compromise is due to chronic inflammation of joints
Etiology-Unknown, multi-factorial, suspect autoimmune, research in bacterial or viral component, RF is Ab specific to autologous IgG, maybe genetic component
Classification criteria- o morning stiffness ( >3 minutes and at least 1 hour until max improvement), o arthritis of 3 or more joint areas, o arthritis of hands joints (wrist, PIPs and MCPs), o symmetrical (simultaneous), o rheumatoid modules, o serum rheumatoid factor (+), o radiographic changes (erosions and body decalcifications)
s/sx-anorexia, weight loss, low grade fever, depression b. radiographic features.
Joint erosion, joint space narrowing and intact articular cortex
Alignment, bone density (osteoporosis), cartilaginous spacing and soft tissue swelling, , joint space narrowing and subchondral bone destruction and cartilage damage d. Describe typical joint distribution patterns of rheumatoid arthritis.
Joint involvement-Bilateral, symmetrical, cardinal signs of inflammation, arthralgia, crepitus, limited hand function
Wrists (flexion contracture limits grip strength, volar sublux and carpal rotation to radius, and deQuervain’s disease-tenosynovitis of first dorsal compartment), Hand joints (symmetric MCP and PIP joint involvement, MCPs have volar sublux and ulnar drift and PIPs have swan neck and boutoniere, DIPs are normally spared), Mutilan’s deformity-severe w/profound functional impairment
Hip-not commonly involved,
Knee-commonly involved due to large amount of synovium, flexion contracture due to pain and guarding (radiograph-diffuse osteopenia, no osteophytes, loss of joint space)
Ankles and feet-pronated hindfoot, hallux valgus, MTP sublux, hammer/claw toes, pain in heel
Tendons-tenosynovitis decreases smooth gliding at sheath e. pharmacologic interventions
Aggressive management at disease onset in order to minimize destruction, NSAIDs, corticosteroids, DMARDs (disease modifying anti-rheumatic drugs), early use and prolonged
(methotrexate, Au)
4. Osteoporosis
Definition-a skeletal disorder characterized by compromising bone strength predisposing to an increased risk of fracture
Pathophysiology-early menopausal bone loss, calcium/vit D deficiency and other factors lead to inadequate peak bone mass, decrease in bone mass/quality, which leads to low bone mass and impaired bone quality which leads to fractures-trauma can lead to fractures as well a. risk factors.
Causes of inadequate peak bone mass-genetic factors, inadequate nutrition (calcium), limited activity, diseases (Cushing’s), drugs like corticosteroids or anti-convulsants that impair bone mass acquisition b. radiographic features.
BMD is measured using the DXA, along with diminished osteoclastic activity
Radiographic images will show less white areas where bone loss has occurred (osteopenic)
hip, distal forearm, vertebrae, proximal humerus
BMD testing-women over 65, women under 65 w/1 risk factor, women under 65 w/fractures, women considering OP therapy, women on HRT for prolonged time, men above 65-70, presence of hypogonadism or alcoholism, use of gluccocorticoids, previous fracture or evidence of bone loss
T-score-DXA-BMD, results expressed as std deviation, compares and individual’s BMD to the mean value for young individuals and expresses the difference in a std deviation (-1 and above is normal, -1 to -2.5 is low BM or osteopenia, and less than -2.5 is osteoporosis)
The t-score should only be used for post-menopausal women; pre-menopausal women should utilize the z-scores to determine if BMD is abnormally low to check diagnosis for secondary causes like glucocorticoid therapy, hypogonadism, hyperthyroidism etc. d. pharmacologic management
Calcium and vitamin D supplementation, and hormone replacement (estrogen)
Antiresorptive drugs-biphosphonates- prevent bone reabsorption, SERMs (selective estrogen receptor modulators), estrogen and calcitonin, anabolic-PTH e. fracture risk reduction and role of exercise
Strength training exercises can maintain/increase BMD and improve muscle mass, strength and balance to reduce the risk of hip fractures
Protective effect of previous physical activity of the risk of hip fractures,
Intense weight training at 70-90% RPM along with weight bearing exercises to load the spine like squats, hang cling and jumping in order to maintain BMD and increase strength
Tai chi-good low intensity training to reduce fall risk with proprioceptive training and reduce bone loss in tibia
5. Diagnostic Imaging a. Understand sensitivity and specificity as it relates to diagnostic tests.
Specificity-low false positive, high false negative, test’s ability to obtain a true negative, the condition is not present (ex=plain films, if you see it, it’s there, but if you don’t it may still be there)
Sensitivity-high false positive, low false negative-the test’s ability to obtain a true positive, the test is positive when the condition is present (ex=MRI can detect very subtle changes in soft tissue, but it doesn’t indicate the nature of any pathology) e. Understand directional labeling of film (AP, PA, R lateral, L lateral).
At least two views necessary in a 90* angle to detect all 3 dimensions
Named for the direction of the beam relative to pt and pt position
AP-anterior posterior, the beam is traveling through in that direction with the x-ray tube in front of the patient and the plate behind them
Alignment-size of bones, number, shape and contour, joint position/alignment
Bone density-dense cortical, less dense cancellous and medullary cavity, less contrast=osteoporosis, increased density where WBing, texture abnormalities (visible trabeculae is normal), excessive sclerosis=DJD
Cartilage Spaces-joint space width, subchondral bone, presence of osteophytes at joint margin=osteoarthritis, assess epiphyses and growth plates
Soft tissue-gross size of musculature, assess outline of joint capsules, assess periosteum g. Differentiate indications of CT vs MRI studies.
CT-cross-sectional x-ray, x-ray tube and film move around fulcrum with equipment or computer, detailed anatomical imaging of bone, sensitive and specific to fracture
MRI-axial/sagittal cross section images, magnetic properties of human tissues respond in a predictive way, images soft tissue well, it’s non-specific and expensive h. Differentiate T1 vs. T2 MRI images.
T1= shorter repetition time and echo time, (1=long bone is bright) good for anatomy
T2=long repetition and echo time, show soft tissue damage, good for trauma (2=H2O is bright)
6. Fracture Overview, UQ, and LQ a. Describe a fracture based on established classifications and descriptors.
Simple transverse
Oblique-heal faster than transverse due to contact and overlap of the fxs, so do spiral
Spiral-spirals down and around the bone
Longitudinal
Comminuated-several bone fragments, trauma
Impacted –ends of bone pushed together, often femur in car accident
Depressed-ends of bones pulled apart
Avulsion-part of the bone gets pulled off because of high force
Cortical bone is more tolerant to compression and shearing and intolerant to tensile forces while cancellous bone is more susceptible to compression fractures
Salter harris classification of growth plate injuries: o Type I-run along growth plate, vital portions remain attached to epiphysis, casting o Type II-most common, along growth plate, take triangle meta frag w/epi, reduction and immobilize-good prognosis for healing o Type III-along growth plate, the perp to the joint, surgery to restore joint surface, good prognosis if blood supply is intact to separated portion o Type VI-from joint, across the growth plate and into meta, surgery for joint surface replacement and to re-align growth plate, prognosis not good unless alignment good o Type V-compression to part of the growth plate, growth disturbance b. Recognize fractures by “common” name, joint(s) and bone(s) involved, MOI and treatment.
Mallet finger (drop finger or baseball finger)-MOI-forced flexion of extended DIP, may have avulsion as well, splinting to avoid hyperextension
Boxer Fracture-4 th or 5 th MC, MOI-punch wall or fist fight,
Scaphoid fracture-, MOI-fall on outstretched hand, pain in anatomical snuff box, AVN and non union are very common
Colle’s fracture-transverse fx of distal radius, hand displaced back and out “dinner fork deformity”, MOI-fall on outstretched hand, osteoporosis or post-menopause,
Smith’s fracture (not reverse colle’s)-fracture of distal radius w/palmar dislocation, MOI: pronation, fall on flexed wrist, young men w/blow to back of hand,
Monteggia-proximal/mid 1/3 of ulna w/radial head dislocation, MOI: fall on outstretched hand or direct blow (MVA),
Galeazzi-distal 1/3 radius fx w/disruption of the RU joint, MOI/Rx: same as above
Radial head fx: MOI: impaction of capitellum on radial head, by a valgus force, axial loading on a pronated and flexed or outstretched arm,
Distal humeral fx: younger than 8, risk for nerve/vascular damage,
Greenstick fx: children, have intact periosteal sleeve
Clavicle fx: fall or direct blow to fx, usually in middle 1/3, fig 8 sling for non-displaced
Femoral shaft fx: high force trauma-MVA- can have muscle damage as well,
Talus fx: large forces from fall from height or trauma impact, prone to AVN, if fall from >3ft it is associated with lumbar spine burst or compression fractures d. Describe potential fracture complications.
Initial-local skin, vascular, neuro, muscular or visceral injuries
Early-local=immediate sequale like gangrene or compt syndrome, septic arthritis in joint, or osteomyelitis (common with hardware) or necrosis of the bone. Remote=PE, fat embolism, pneumonia or tetanus
Late-local=stiffness or traumatic DJD, Bone-abnormal fx healing like malunion, delayed or nonunion, growth disturbance from epi injury, persistant infection, post traumatic osteoporosis,
CRPS, re-fracture Muscular-post traumatic myositis ossificans=joint mice, late rupture
Compartment syndrome-increased pressure w/in fascial compartment (ant leg) due to edema or hematoma in closed space. S/s-pain, edema/tight, pulselessness** can become chronic due to muscle expansion or decrease size of comp, emergency situation
Heterotrophic ossification-joint ossification, periarticular, elbow and hip most common, etiology is unknown, often seen in ICU wound, neuro and sepsis pts, long bed rest. Aggressive ROM is important e. List factors determining time of fracture healing.
Age of the patient (birth=3wks, 8=8, m12=12 and 20=20)
Site and configuration of the fracture-surrounded by muscle heal faster, cancellous bone
Extent of initial fracture displacement-non-displaced w/intact periosteal sleeve heal 2X faster
Blood supply to bony fragments-if both have blood supply=excellent px, if one has blood supply it can be immobilized and serve as a host for the other segment, avascular=have to have some kind of re-vascularization f. Describe surgical and/or medical management options for fractures.
Open reduction- go in surgically, comminuated always need open
Closed reduction-same as popping a finger back into place
Immobilization-casting/splinting, internal fixation (pins, needles, screws ect), or external fixation which is the highest degree of fixation
PT intervention-consider age, MOI, functional demands, immobilization, ortho POC, exercise, mobility, ADLs, wound care, and education
7. Hip Fracture
Intracapsular-femoral head and neck, high rate of non-union and AVN, can have a hemi or THA
Extracapsular-trochanteric (avulsed young athlete), inter-trochanteric (elderly, btw trochanters), subtrochanteric, need open reduction and internal fixation b. Describe the potential complications of hip fracture.
CV, pneumonia, pressure ulcers, delirium, UTI, wound infection, depression, malnutrition
DVT-60% w/out prophylaxis, drops to 20% with it, need to mobilize and apply TED hose immediately
PE: 10-15%, mortality is 2-10%, 14% of deaths due to hip fx c. Distinguish delirium from dementia and describe its implication to recovery.
Delerium is temporary insanity (confusion, disoriented to time/place, incoherent, mind wanders) , it is the number one predictor for mortality after a surgery, d. Describe components of medical (non‐surgical) management, indications and contraindications.
Indications:Uunstable med status, non-displaced fractures, or surgery risk >immobility risk
Pain control, reduction/fixation in good position, return to function, prevent complications e. Describe and contrast surgical options (ORIF including pinning, nailing and use of compression plating, hemiarthoplasty), indications and contraindications.
ORIF-pinning, nailing, IM rod, bone conserving, lower mortality, high failure, younger/active pts, mainly for extracapsular fx
HA-intracapsular fx, better outcomes than ORIF, lower failure, 5% dislocation, functional deterioration 3-5 years o Bipolar-femoral head articulates w/acetabulum AND stem o Unipolar-femoral head articulates w/acetabulum but is fixed to stem o Cemented=higher intra-op morbidity, more stable initially, may crack and prosthesis will fail, may cause osteolysis, quicker rehab initially, good bc bone doesn’t grow over 1-
2mm gap, PMMA can cause excessive joint wear and subsequent revision is difficult o non-cemented= poor function, allows for bony in-growth, but implant must closely fit the channel, protected WBing period, younger athletic people, decrease operative time, bone conserving and no fragments, but cemented has better short/mid term outcomes w/no long term
THA-intracapsular fx, skill is key, outcomes >3years, dislocation 5-10% risk, can fix complications from ORIF or HA
o Posterior-increase infection/DVT, and dislocation, no hip flexion past 90*, no IR or adduction past midline o Anterior-increased op time, infection and blood loss, no extension, ER or abd f. Formulate a PT plan of care based on a clinical scenario.
Early mobilization is crucial
Subjective-pain, prior home/social situation, what their goals are, orientation (day, time, season, where, name)
Objective-ROM, strength, incision, dressing, check heals for pressure sores, vitals before they stand, sensation
Acute treatment-based on WBing, heel slides, ankle pumps, short arc quads, may be able to get up to chair, 2 nd visit you may be able to work on gait, only closed chain w/WBing
Sub-acute-closed chain activities, chair sitting and walking
Home-address cause, make home modifications to reduce falls
8. Total Joint Arthroplasty
Goals: restore function, reduce pain, gain muscle control/strength, return to prior functioning a. List the primary (2) indications for total joint arthroplasty.
Marked pain and decreased function b. Recognize contraindications and appreciate selection criteria for total joint arthroplasty.
Infection (#1), poor health, severe/uncontrolled HTN, progressive neuro disease, dementia, latent renal or respiratory insufficiency
Obesity and diabetes pts often receive totals
DVT, PE, chronic infection, arthrofibrosis, and CRPS (last 2 not common), components loosen, allergic rxn, mal-alignment, fracture during surgery (common w/revision), hematoma, pneumonia, leg length discrepancy, neural injury, dislocation, HO, thermal damage/laceration e. PT plan of care
Early post-op: educate about precautions, positioning and ice, exercises-AAROM, AROM, strengthening w/ankle pumps, heel slides, isometrics, SAQ/LAQ, active abduction, progress to closed chain ASAP (SLR requires caution)
Sub-acute-bed mobility, transfers, gait, car transfer simulation, stair training, emphasize compliance to precautions, equipment planning (assistive devices and commodes), D/C planning and recommendations
Late-functional training, strengthen hip extensors and abductors, wean assistive device, limit high impact w/rotation activities f. Understand functional mechanisms of THA dislocation.
Preservation/size of the femoral head component (22, 26, 28 or 32 cm)-smaller head is less stable with more ROM you have a greater risk for dislocation
Combination of movement patterns during loading-rising from low surfaces, twisting the trunk w/feet planted on the ground, bending down to feet from a seated position (putting lotion on is very common MOI) g. Discuss risk factors for dislocation.
Bending down to put lotion on leg-flexion, adduction and IR
Re-current dislocation-may require spica casting and WBing restrictions, education for ADLs and home evaluation along w/family communication is important h. Differentiate between THA and bipolar hemiarthroplasty.
Bipolar hemi-native acetabulum remains w/cartilage, metallic cup placed in native acetabulum,
THR-total hip re-surfacing, metal on metal or BHR, just acetabular component w/cap on femoral head-younger more active pts, rapid recovery and return to high functional level, more stable, bone preservation, i. Understand the indications for high tibial osteotomy, unicompartmental knee arthroplasty, and total knee replacement.
High tibial osteotomy-change alignment of joint, younger pts to delay need for TKA,
Unicompartmental-minimum knee flexion of 90*, no significant flexion deformity and <15* varus/valgus deformity, mobile patella, intact tibial plateau and femoral, and satisfactory ligament stability, normally for end of range ages, often in older, but recent in young, high failure w/obese, bone conserving, shorter post op than TKA w/8-10 year survival
TKA- ACL is excised, PCL can remain or be excised, and collaterals are saved, j. Formulate a PT plan of care for a simulated total knee arthroplasty patient
Acute-ice/positioning, maybe CPM, d/c goal of 0-90* ext/flex (includes PROM-document), isometrics, ankle pumps, heel slides, SAQ, LAQ-assist, SLR
Acute to sub-acute-mobility: gait training, esp normalize to achieve functional ROM, education for WBing precautions and importance of quality of gait, edema and pain management, d/c planning and recommendations
Late intervention-functional activity, increase ROM w/modalities and soft tissue mobs, strengthen, muscle control and balance, limit high impact and rotational activities
TKR-more common than THA, longer rehab, must be WBAT on B LE, can be staged or same time,
THA-staged at least 1wk, increase DVT risk, bilateral post hip precautions difficult
Prognosis-depends on comorbidities, attitude, and rehab participation/intensity
9. Rheumatology
Gout: rapid onset, pain/inflammation at joint, *1MTP, knees and ankle Etiology: alcohol, hyperuricemia, pseudogout by local production of calcium pyrophosphate dehydrate crystals, more common in men, treat inflammatory response not crystals w/NSAIDs and gluccocorticoids,
PT can work w/ROM
Juvenile RA: pauciarticular <5 joints involved, polyarticular>5 joints, systemic=fever, multiple joint involvement, linear growth retardation, osteopenia, cardiac involvement, PT can strengthen when not in the acute phase, disease management: pt/family education, NSAIDs,
DMARDs,
Systemic sclerosis (scleroderma): localized is characterized by fibrotic skin lesions that are not associated w/internal organ involvement, early sx are diffuse and non-specific like fatigue, body aches, arthralgias, stiffness, cold sensitivity, finger swelling and heartburn, skin inflammation and hardening-autoimmune
Polymyalgia Rhematica: , systemic inflammatory disorder in indiv >50, multifactoral, diagnosis by rapid, remarkable response to low-dose corticosteroids, aching in elderly, proximal symptoms-neck, spine and hips
10. Fibromyalgia a. Describe the typical clinical features of fibromyalgia and diagnostic criteria.
Syndrome of widespread body pain, over 3 months, 11 of 18 tender points on both sides, more prevalent in females ages 30-60
s/s: sleep disturbance (due to hormone imbalance), depression, anxiety, morning stiffness, headache, N/T, temperature sensitivity
DX: rule out other rheumatic factors 1 st , 3 months of widespread pain w/11 of 18 tender points, bilateral side pain UE/LE, and characteristic features
Tender points-lower cervical region (over SCM), second rib, occiput, trapezius, supraspinatus, lateral epicondyle, gluteal greater trochanter, knee
Pathology-musculoskeletal (abnormal muscle fibers and energy metabolism), endocrine
(hormone imbalance/poor healing), CNS, immune system (up-regulation of inflammatory markers) b. Specify PT intervention parameters for exercise and conditioning.
Subjective exam-thorough pt history, clear whole body chart, family history for CFS, nagging deep trigger pt pain
Objective exam: asses pain, tenderness, sensory and functional tests for goals, only use 4kg of pressure on trigger pts when testing
Intervention: multi-disciplinary, pain management (analgesics, NSAIDs, anti-depressants,), stress release techniques, physical activity, sleep disorder, nerve pain
Education-chronic but not progressive, debilitating if you don’t continue to function, psych referral for depression, anxiety, alcoholism
Exercise-improve function/energy level not reduce pain! Aerobic-endurance, something enjoyable, low impact, gradual increase to 30min most days at 60-70% max HR, Strength-start low, 1-2lbs, few reps per set like 3-5, add sets slowly, avoid eccentric, long relaxation, alternate days and muscle groups, Stretching-daily, warm-up or cool down, least effective when performed alone
11. Systemic Lupus Erythematosus (SLE) a. Recognize characteristic clinical features and systemic involvement of SLE.
Variable presentation: butterfly rash on face, musculoskeletal, dermatological, renal and hematologic, unexplainable fever, ryanauds, swelling, joint inflammation, malaise, fatigue, bloating and overweight, chest pain and hair loss
Women 20-30yo, multi-organ, autoimmune, may have genetic factor but not familial, environmental triggers like UV exposure
PT for acute care and functioning at work, pt education and health maintenance, avoid UV light,
NSAIDs, anti-malarials, IV IgG, immunosuppressors
12. Ankylosing Spondylitis a. Describe the clinical presentation of early and late ankylosing spondylitis.
Axial skeletal involvement including S1 inflammation, gradual loss of mobility, lumbar spine flattening, thoracic kyphosis, fusion of cervical spine, young men <45, sometimes @20yo, genetic/autoimmune
13. Bone Malignancies and Metastatic Disease
Osteosarcoma-<20yo usually, over ½ the cases are in the metaphysis of the distal femur or the proximal tibia, unknown etiology maybe due to radiation exposure, metastasize to lungs and other bones only o Medical management-, biopsy tumor for malignant cells, pre/post op chemo, surgical excision of affected bone (80* of the time no amputation), 70* long term survival w/metastatic disease
Ewing’s sarcoma-ages 3-25, 60% appear in LE or pelvic girdle, mets to lungs and other bones, present w/low grade fever, anemia and pain o Medical management-onionskin appearance of cortical bone, mixed, multi-drug pre op chemo, surgical resection has replaced XRT post op chemo for 1 year, 75% survival of 5 years
Chondrosarcoma-over 50, central skeleton esp. the pelvis, low grade, hard to distinguish from benign cartilage disease, characteristic radiographs o Medical management-surgical, chemo and XRT are reserved for the progression of disease, excellent prognosis w/low grade disease b. Recognize indications and comparative evaluation of limb sparing vs. amputation (from a functional perspective).
Limb sparing-success against survival rate and function achieved through amputation
Physical challenges like maintaining activity level, psych/social maturation, body image, and self-esteem issues, recurrent hospitalization and multiple surgeries, vocational issues, and lifelong insurance to keep up w/prosthetic and rehab
Acute PT intervention-mobility training, bed mobility and transfers, strengthen w/precaution,
ROM w/precaution, gait training w/protective WBing, endurance
Late-joint function, strengthening, quality and efficiency of gait c. Name the 5 most common primary malignancies that metastasize to bone.
Prostate, thyroid, breast, lungs, kidney (P T Barnum Loves Kids) d. Distinguish osteolytic and osteoblastic lesions and recognize radiographic features of each.
Osteolytic-destruction of bone by stimulated bone resorption
Osteoblastic- dense, new bone growth w/likely lytic processes and compromised bone quality e. Describe the following interventions for the high risk pathologic fracture: PT training for unloading, pharmacologic (Biphosphonates), XRT, surgical, orthotic
Pathologic fracture-severe complication of osseus metatastic disease,
Protective unweighting prescription-evaluate integrity of structures w/proposed weight redistribution, prophylactic repair is controversial, may not determine fracture risk
Mirels- 4 variables-site (UE, LE or peritrochanteric), nature (blastic, lytic or mixed), size, and
Pain (mild, moderate or functional)
More fractures occurred in pts that were on bed rest than in pts w/therapeutic exercises
Rehab-active pain free ROM, no PROM, no resistive, limit MMT to uninvolved side, educate on risks of bed rest
Hip/pelvis and LE-Surgical-IM rod or bipolar prosthesis, early WBing and compressive/rotational force tolerance, gait training w/assistive device, strengthening
Non-operative-unloading and minimize stair climbing
UE-fracture brace, IM rod for large humeral lesion, compression plate or cemented prosthesis of humeral head, prophylactic fixation for use of assistive device, consider WBing demands, Early
AROM and distal ROM for edema management f. Multiple Myeloma
Patho- B-lymphocytes transform into malignant cells that resemble plasma cells and proliferate, abnormal cells accumulate in the bone marrow and cause a tumor
The cells stimulate osteoblastic activity causing lytic lesions in ribs, t-spine, pelvis, humerus, sternum, skull and others
As these cells multiply they weaken the bone causing pain and fractures, g. Discuss the role of the physical therapist in the management of cancer.
PT: back pain, compression fractures are common, spinal orthotics, AROM, maintain ambulation
14. Acute Spine Management
3 column Spine stability:
Anterior: Ant long ligament, anterior2/3 of vertebral body and annulus fibrosis
Middle: posterior 1/3 of vertebral body and annulus
Posterior; posterior lig complex and vertebral arch structures
Fracture 1 comlumn=stable, all columns=unstable, 2=if middle is stable the injury is stable a. Describe medical and/or surgical management of upper and lower cervical spine fractures.
40% have neurologic involvement
Stable-don’t have bone/joint displacement eg: compression fx, traumatic herniated disc, unilateral facet dislocation
Unstable-potential for significant joint displacement, fracture-dislocation or bilateral facet joint dislocations
Cervical Fracture-traumatic impact, MVA or fall, avulsion, compaction or impaction, large cord space, high mortality above C4 due to respiratory involvement o Surgical stabilization-post plating w/or w/out constructs, anterior plating, combo of anterior/posterior, post has greater stabilization
Occipital condyle fx-rare, just halo stabilization, rarely requires surgery
A-O injuries-rare known survivals, neuro involvement, halo stabilization, chronic=fusion
Atlas Fracture-50% assoc w/dens fx or others, compressive force or true “burst fx”=Jefferson
Fracture, transverse lig tear or avulsion, rarely neuro involvement, halo
Dens Fx: bimodal distribution w/OP in elderly, , high non-union, other fxs common, halo or other rigid immobilization, surgical if there is neuro component
Axis Fracture-Hangman’s-traumatic spondylolithesis-bilateral interarticularis fx, MVA w/hyperextension, not associated w/neuro unless distracted, surgical stab, halo
Lower cervical spine: assumed until proven otherwise, corticosteroids, and stabilization for all cases w/neuro after re-alignment, *anterior decompression
Distractive-flexion-MVA, fall or contact sports-most common-C5-6-7, uni or bilateral facet dislocation with compromised posterior long lig, closed reduction, ant/post stabilization
Vertical Compression fx: MVA/diving, C5,6,7, compression/shorten anterior and mid columns, post stabilization, rigid-halo
Compressive-flexion-teardrop-assoc w/facet dislocation, lig rupture or disc tearing, extreme force, ant/post stabilization and rigid immobilization
Lateral Flexion-MVA, lateral blow, C-collar, minimal findings, no lig damage, no surgery b. Describe medical and/or surgical management of thoracic and lumbar fractures.
Thoracic spine-bimodal distribution, compression, mets disease, traumatic, flexion forces normally contribute, transitional vertebrae T1-4 and T9-12, T12-L1 most frequently involved
Management: depends on rib, sternal involvement, loss of vertebral height, instability and spinal cord compromise
T12-L1 so common bc T-spine is rigid while L-spine is flexible, transition zone to cauda
Compression Fx: failure of anterior column, low risk of neuro comp
Burst fracture-axial loading, common to have neuro comp
Seatbelt (flexion/distraction)-transverse fracture line
Lumbar: T11-L2 is most susceptible, hyperflexion w/ or w/out shear rotation when fixed, seatbelt in car accident MOI, *hindfoot fractures are often associated, Surgical stabilization if lumbar kyphosis is present, L2-L5 are stable due to size/muscle, L5-S1-unstable, injury
Treatment-surgical if instability and/or neuro comp, molded jackets, braces, corsets, rigid=TLSO, may have hip spica attached c. Describe post‐operative (acute) PT intervention of trauma/surgical spine patient.
Focus on mobility not strength, progressive w/neuro d. Select appropriate mobility activities and strategies for simulated patient with an acute spinal
Log rolling activities, avoid flexion/rotation w/ADLs, assistive device for early amb, Late rehab if rigid orthotic is discontinued and they still need therapy
Scoliosis Intervention: conservative bracing and PT, surgical after growth, Idiopathic vs neuro
Post-op: early device for ambulation, late recovery/return w/some activity limitations
15. Splint and Orthotic Overview
3 point pressure system: produce moment or torque at the joint, forces have intended or unintended effect over time, longer the distance from the joint of the application of force the greater the moment at the joint, long term will affect the resting length of the muscle, change force production and influence function b. Define terminology related to orthotics.
Static-one position, serial static-change position every month or so, dynamic-elastic mobilization (plantar fasciitis splint), static progressive-adjusted as you go, more load than a serial static
16. UE splinting
Hand:
Extrinsic muscles=flexors/extensors
Intrinsic muscles=hypothenar/thenar, interossi, and lumbricals
Extrinsic extensors have more risk of shortening, so worry about DIP flexion with PIP extension, bc the extensor mechanism relies on excursion of the tendons, it is less for extensor tendons than flexor tendons, it is also harder to compensate for extensor shortening
Arches: maintained by intrinsic muscles, Proximal transverse-stability for finger flexion, Distal transverse-for thumb opposition, Longitudinal arch-allows palmar arch for holding pencil
Function: dependent on proximal stabilization, wrist, forearm and hand function as one unit with wrist being the fulcrum
4 Phases: reach, prehension, carry, release a. Describe a resting hand splint and the rationale for its use.
Functional hand splint: 20-30* extension, thumb in palmar abduction, MCPs in 15-20* flexion, IPs in slight flexion, because it is the most functional position of the hand and wrist b. Describe the intrinsic + hand splint and the rationale for its use.
Intrinsic +: MCP flexion w/DIP/PIP extension bc MCP extension causes slack in the collaterals and risk of shortening and PIP flexion causes slack in the volar plate, risk of shortening so it’s the anti deformity splint o Palmar burn: wrist 30-40* extension, dorsal: neutral-slight extension, crushing injury: 0-30* extension o MCP: burn=70-90* flexion, crushing=60-80* flexion IPs extended and thumb abducted
Intrinsic -: PIP/DIP flexion, MCP extension, often due to ulnar N palsy bc the extrinsic extensors are unopposed
Extrinsic stability-we can strengthen, intrinsic stability-ligamentous and disc problems that we cannot fix
18. LE Orthotics
MMT-focus on general muscle groups and functional strength, keep the orthoses as minimal as possible so they maintain the function that they have
Rigid deformity still needs to be accommodated so that it doesn’t collapse further
Dropfoot=stroke, CMT, MD, PF contracture is common bc position of comfort and anterior tib doesn’t work to pick up foot
Pathologic gait:
DF-terminal stance and swing, unilateral paralysis they will have excessive hip/knee flexion, limp and decreased swing on affected side=DF assist, post leaf spring AFO, hinged plastic w/Gillette ankle joint, metal w/springs posterior, PF stop if they have hyperextension at the knee
PF-pre-swing, toe off-PF stop, metal bar in front, full foot plate on plastic
Quads: IC, unilateral paralysis-stairs, anterior lean to move COG anterior to knee jointto stabilize, often push thigh back with the hand, DF stop KAFO (no quad)
Genu recuvartum: set at 90*, pt can push through, can control with AFO a. Apply the biomechanical principles of LE orthotics.
3 point pressure: KAFO for unstable knee to block out flexion, AFO: sagittal, shoe is the force on the dorsum of the foot, drop foot-allows for some PF/DF, single bar lateral upright=pes planus, club foot-a progressive serial cast immediately to truly correct the deformity d. Recognize indications and limitations of LE orthotics: AFO, KAFO, posterior leaf string.
Motion: ASAP when they have no instability bc they will use more energy and have more deformity if we continue the use of the orthoses
AFO-adds stability during stance, may add gait deformity
Posterior leaf spring AFO-similar to prefabricated, controls DF during swing, no medial/lateral stability, doesn’t control knee bc they can PF through the plastic (set at 3-5*
DF)-least restrictive, similar to plastic DF assist
Semi-rigid AFO-forward, medial/lateral stabilization of STJ, can’t PF at heel so knee flexion moment occurs, helps prevent knee hyperextension, trim lines bisect the malleoli, allows for
DF in late stance
Solid AFO-trim line anterior to malleoli for max med/lat and sagittal stability o Full length footplate extension: prevent toes from curling and hyperextension at the knee o Solid ankle dynamic AFO-PF block, extended medial forefoot trim to control the forefoot o Spina bifida: as they get older progress to w/c to conserve energy
Paralysis of DF/PF: lateral lean, circumduction, excessive hip flexion, hang w/swing, decreased stance no push off, regular stance on unaffected side
Articulated AFO: weak quads they will buckle so they must have good quad strength
Metal-calf cuff to adjust, good for edema bc it’s open, atrophy can adjust to, insensate bc shoe is cushioned so diabetic foot ulcer is common, not good bc it’s heavy, less control bc it’s not total contact, and cosmesis o Components: shoe, stirrup, ankle joint (free moving, DF assist or double action), side bar-single or double, calf band and cuff, varus or valgus corrective straps optional o Double action-springs or metal bars in channels, DF weakness of ant tib tehn the spring goes in the posterior channel so you can DF when you are unweighted, PF assist-spring in anterior channel-DOESN’T EXIST, metal bar in posterior channel will give a knee flexion moment and no DF stop
Patellar tendon bearing orthosis-screws on sides of metal bars can raise up the LE, to unweight for an ulcer on the heel or midfoot
Charcot retaining orthotic walker-best for unweighting o Charcot foot-diabetic, pes planus, active, gets hot/swollen, insensate foot causes microtears every time they walk=rocker bottom foot (arch goes opposite way), which leads to ulcer on midfoot, orthotic provides 2 layers of foam, total contact, removable so you can check the wound, when swelling goes down they can be casted
KAFO-extension of AFO, can be cut down as they get better, have different joints, extra screws on peds so that they can adjust as they grow o Free joint-medial lateral instability o Variable ROM-the ones you wear after ACLs w/goni on side o Posterior offset-move mechanical angle posterior to decrease lean, increase stability, for weak quads o Drop lock-retainer, ball bearing w/spring, can unlock for part of day w/stability then lock when they get tired o Bail lock-lever goes up to unlock, so at chair level the chair will unlock it to sit
Stance control KAFO-locks knee with WBing, unlocks during swing-LLD and circumduction o Provides stability in stance, movement during swing, reduces gait deviations and energy expenditure o Ideal patient: isolated quad weakness, SCI, uni/bilateral paralysis, polio or post, MS, stroke, and MD o Hip extensor and flexor strength needs to be 3-5, w/1-2 they will need additional gait training and compensation, w/weak hip extensors they may need DF stop for knee extension
o Contraindication: knee flexion contracture greater than 10-15*, spasticity, incorrectable varus/valgus greater than 15*, poor balance or ataxia o Advantage=stable, disadvantage=high energy expenditure, enduces gait deviations, uneven stride, longer affected limb, excessive wear/tear on contralateral limb joints
Stance control benefits-reduce energy expenditure and gait deviations, increase CO and mobility/activity level
PT indication: isolated quad weakness, doesn’t block ankle ROM to support knee, but hip flexor strength must be 3-5
Can’ t be used if they have a knee flexion contracture>10*
Weak quads=over time increase in hyperextension, circumduction, lack DF, hip hiking, contralateral heel rises (w/post polio they have been hyperextended for so long we can’t completely correct it) e. Select the appropriate orthotic based on a simulated patient scenario.-LAB
Shoe needs to have a chushioned heel that is forgiving so that you don’t have an extended flexion moment
Carbon fiber AFO (same as post leaf spring)-DF assist only, very active people, isolated transient foot drop, peripheral nerve injury, light weight, nerve palsy
Carbon fiber Pre-tib AFO (custom fit)-can build up arch support, rigid, no PF, closed chain won’t allow DF, looks like a floor rxn AFO, shin anterior shell give extension moment at the knee in stance for weak quads so you can’t lock your knee (3 point pressure system)
Common weakness pattern with neuro=weak ant tibs and quads
Plum line=hip/knee/ankle stacked for stability, with knee in front of the line the quads will be continually firing, with knee behind the line the quads can relax and hamis fire so that you can’t buckle your knees
Metal upright=strap 2 fingers below the fibular head, posterior channel goes up diagonally to anterior channel, if there is just one channel it is always the post channel, ball bearing goes in first, then the pin or spring, then a screw on top (the pins can wear down)
Pin in spring=2 coils of functional spring is pointless bc you don’t have a recoil
Spring=posterior (load PF, open DF), anterior (load DF, open to give you PF)-almost never used
Pin=posterior (block PF) anterior (block DF)-you can block both for stability w/slight ROM for DF/PF for walking
PF stop will limit foot drop and knee hyperextension in stance-incomplete SCI recover quick, but they must have quad control to give them the DF
Progression: solid ankle-5* DF/PF (still can’t buckle)
Posterior spring-DF assist, plastic orthotic would be the post leaf spring-can’t place anterior pin with in or you will lose the effect
T straps-pt has so much tone in PF/inv contracture so you put them in double upright and pull the straps to correct it
ALS-UMN, spasticity, carbon fiber pre tib (off shelf) brace AFO, good bc they are lite and good for people that are weak, can have after 1 clinic visit, allows for edema
Walk aid-unweight hell, e-stim fires ant tib to DF foot, it re trains the muscle only during stride (DF assist like post leaf spring), but doesn’t help in stance
ALS can’t re-edu muscles bc they are denervated
Checkoff-2 on AFO for DF weakness and DF weakness with knee instability
Contraindication for spring assist-don’t use w/spasticity, but you can use it to gain a normal stance
Parkinson’s gait-spastic gait-orthotics substitute for things that aren’t there, can’t take away
19. PT Management s/p amputation a. Recognize the predominant risk factors for amputation.
Men have a predominant risk for traumatic amputation due to occupational hazards, vehicle, violence or burns-farmers-16% trauma
80% of amputations are due to vascular disease-bilateral amputation risk is high (25-45%) so skin checks on the unaffected limb are important
5 year mortality: due to PVD, renal disease, and age
Peds-most non-traumatic amputations, cancer usually osteosarcoma, children get into prosthetic faster but you have to consider growth b. Define terms describing amputation and congenital deficiency.
Trans-amputation across the axis of a long bone
Partial-amputation of foot distal to ankle joint or hand distal to wrist
Disarticulation-amputation btw long bones, anatomically through the center of the joint
Osteomyoplastic flap: prior to amp, an osteoperiosteal flap is made to be sutured to the remaining periosteum to cover the bone and plug the marrow cavity then in neutral the antagonist muscles sutured across the bone ends-ERTL procedure
Myodesis (muscle to bone)-distal transected muscle are attached to bone through drill holes at the distal ends of the bone, muscles attached at a point of moderate tension to become fixed along their normal pathway and slightly beyond their rest position in order to have max function
Tenodesis (tendon attaches to bone)
Myofascial-muscle to fascia fixation
Myoplasty-muscle sutured to antangonist muscle
Muscle needs to maintain length so no atrophy or contracture, needs distal attachment
Bone is beveled and smoothed at the end to be covered w/soft tissue
Flaps by skin and muscle must be longer than the limb, suture line is normally anterior with a posterior flap so WBing and prosthetic wear won’t be impeded c. Distinguish between phantom limb pain and phantom limb sensation and list PT interventions to address both conditions.
Post op complications-contractures, edema, phantom leg pain/sensation, depression, grief, pain, infection, respiratory compromise, DVT
Phantom limb sensation-painless awareness of the amputated part, mild tingling, often an incomplete sensation, 90% of pts experience it and usually persists throughout life
Phantom limb pain-constant, intermittent and varying intensities, postural cramping or squeezing, burning or sharp shooting pain, suspected 30-75%
Etiology: common with crush injury or amputation in later life
PT interventions: TENS, US, icing, exercise, compression, massage, desensitization, pt edu of limb handling and use
Scar management: early gentle massage and handling of the residual limb, scar massage and deep friction massage after the incision has healed, educate pt on massage of the residual limb as an adjunct to skin inspections, scar maturation continues for up to a year and skin integrity and pressure tolerance is ~40% of what it was d. Contrast methods of limb edema control: ace wrapping, shrinker, rigid removable shrinker.
Rigid dressing-immediate post op fit w/ prosthetic sock, attachment at distal end that allows for foot and pylon for partial WBing aka IPOP=immediate post op prosthetic o Pros-limits post op edema, decreases pain, increases wound healing, allows WBing early, prevents contracture, protection, earlier into definitive prosthesis o Cons-careful application, doesn’t allow for wound inspection, close supervision
Rigid removable dressing-after sutures/staples removed, polypropylene cast is made from the impression of the limb, worn over compression socks or dressings o Pros-allows skin inspection, continuous compression, protection easy to don o Cons-new fitting when pt gets to 15 ply of socks
Semi-rigid dressing-paste compound of zinc oxide etc, aka unna dressing o Pros-effective edema control, adheres to skin, no suspension, allows ROM, doesn’t trap heat or moisture, inexpensive, easy to contour o Cons-loosens as edema reduces, less rigid than plaster
Soft dressing-wound care for protection and absorption, elastic wrap or shrinker o Pros-inexpensive, light weight, available, washable shrinker o Cons-frequent re-wrap for pressure, breaks w/mvmt/activity, replacement w/change in limb size or stretching, effective, tourniquet effect, doesn’t control position, pt cannot get it on
Ace wrapping-reapply every 4-6 hours, distal to proximal pressure gradient,
Shrinker: elastic sock that helps to decrease edema and help shape the residual limb, it creates a pressure gradient-distal, less proximal, above the knee will require a waist belt to keep it on, size based on circumference and length, used prior to prosthetic fitting and before prosthetic wearing, wear 24 hours a day and continue to check skin
Socks-used for skin protection, friction absorption and to fill the socket volume, it absorbs perspiration, allows socket fit/contact, only used with prosthetic (cotton, wool or blends), 1,3,5 ply, if you get up to 15 ply you have to get a new socket, f. Describe the progression of rehabilitation s/p amputation and factors that are considered.
Pre-prosthetic evaluation: stretching/strengthening, wrapping/shrinker, transfer/gait training, skin/scar mobs, desensitization, protection
Pre-gait training: with parallels bars practice sit <>stand and single leg support, same with assistive device and practice controlled step protecting the involved leg, crutch ambulation is good for pre-prosthesis for conditioning and balance training, provides a better transition than a walker which halts momentum and the COG progresses forward
Rigid dressing with a pylon allows for limited WBing and early ambulation, transtib is casted with knee extension which will limit the quality of gait
Temp prosthesis: initiate gait training, integrate with functional tasks
Positioning: ROM as soon as surgeon allows, get pt prone as soon as medically feasible, initiate wrapping when surgeon allows and monitor application, optimize position w/OOB activities, monitor edema and limb fluctuations
Exercise: o Strengthen: hip extensors/abductors, knee extensors/flexors, closed kinetic chain o ROM: hip extension/adduction and knee extension
Early gait training: single leg ambulation with crutches or walker
Gait Progression: standing-single leg standing
Dynamic activities: lateral, AP weight shifting, stepping side and forward/backward, step ups and braiding
Advanced gait training: reps of gait components, step up down for stabilization over prosthesis, then step over gait for transtib amputee, resisted ambulation, running, jumping, floor-stand, uneven terrain, curb/stair, reach to floor, lifting/carrying
Prosthetist makes all changes in the prosthetic if the fit changes, not PT job
Endurance training: o Energy expenditure: transtib=20% increase, transfemoral=49-65%, B transtib=less than transfem, B tansfemoral=280% increase, hip disartic=200% increase, level and etiology are factors
o Conditioning program: UE ergometer, progressive ambulation, stationary bike w/contralateral LE
Transfer training: POD 1 if pt is medically stable o Stand pivot w/assistive device or use a transfer board if indicated o Transfer prosthesis: for non ambulatory transtibial amputee with sensation, vision or balance defecits o Single limb activities important, esp for transfemoral amputees
W/C: consider if pt is at risk for skin breakdown or socket intolerance o Offset rear axis, power systems, anti-tip extensions or weight front (temporary) o Special cushion for long term transfemoral esp if they are bilateral o Solid seat for short term transfemoral amputee g. Prognosticate the outcome for a patient with a amputation based on a scenario.
Level of amputation and pre-surgical function are best predictors of prosthetic potential
Unilateral transtibial: can be functionally independent at any age
Bilateral transtibial: can be fully functional at “young age”
Unilateral transfemoral: will be difficult to regain upright tolerance w/prosthesis for elderly
Bilateral transfemoral: most are not prosthesis users
Contraindications: dementia, institutionalized, bilateral transfemoral with poor transfer/standing tolerance, previous transfemoral on contralateral LE, unacceptable energy expenditure for ambulation, ambulation function may be compromised by prosthesis (hemipelvectomy)
Residual limb requirements: incision healed w/approximated edges, no infection or drainage, WBing tolerated, frequent skin inspections
Prosthetic selection: based on age, activity, vocational demands, funding and compliance, definitive prosthesis is chosen by prosthetist, MD, PT and patient input/perf w/temp
Temporary prosthesis: shapes to residual limb, early gait training/independence, evaluates potential use of prosthesis, endurance training, prevents dev of contracture w/ambulation, not for full time wear, can have up to 15 ply socks under prosthesis, definitive socket after volume has stabilized
20. Prosthetics
Dysvascular Prosthetics: PVD, smoking (decreases circulation), geriatrics
Irreplaceable loss of blood supply to diseased or injured limb=only indication for amputation regardless of other conditions
Must monitor CV response
Socket: can be replaced if the fit has changed but the components are still in good condition, often happens with an endoskeleton prosthesis
Socket fit-suction=highest degree of fit, suspension and security, difficult to don
Sock or liner fit=order: sock, liner, socket a. Recognize the factors that are considering in selection of prosthetic components.
Foot failure: socket and alignment must be set properly, improper forces may cause premature wear, activity level/weight changes since initial design, foot abuse (walk w/out shoes, improper heel height, water damage, dust/dirt, lack of maintenance)
Knee-height, weight, functional age
Knee failure=socket not aligned, improper interaction of forces=wear, change heel height=added stress to knee, inappropriate use, and all same as foot b. Describe the basic function of the following prosthetic components:
SACH foot-solid ankle cushion heel, simple design, least cost, lowest function. Cushion heel to compress on heel strike, rigid heel to resist during mid stance, flexible fore foot for roll over capabilities
SAFE foot-stationary attachment flexible endoskeleton, L2 pts going on uneven terrain, flexible internal keel permits tri planar movement and easy roll over, stiff and stable for stance
Multi‐axis foot-PF/DF, inversion/eversion, axial rotation, un-even terrain, F3, absorbs gait torque to reduce shearing forces on residual limb o Foot won’t actively move to position but WBing you can move it
(energy storing) Dynamic response foot-internal keel structure, absorbs energy during mid and terminal stance, releases energy at pre swing for more smooth and more energy efficient gait, light weight and durable
Single Axis foot-provides PF and DF motion, stable at heel strike** for above knee amputees and hip disarticulation, bumpers can be adjusted and exchanged to modify foot response, good for F1 F2
Special activity foot: accommodate the unique/specific demands of sport and athlete, customized can only be used for one activity or sport
Foot enhancements: o Vertical shock abosorber: built into foot or separate component, reduces impact during stance and heel strike, reduces sheer within the socket, improves rotation at heel strike o Rotational Torque absorber: built in or attached separately, absorbs gait torque to reduce shearing on the residual limb, rotation mobility for standing and twisting movements, good for factory workers and bilateral amputees o Heel height adjustable foot: maintain uniform distance from the heel to the knee center-not covered by insurance
Knee-, F3 in feet is dynamic response foot, F3 for knee we can use hydrolic and pneumatic knees to adjust to cadence
Knee Selection-stability and function, F1/2=fixed cadence, 3/4 =dynamic cadence
Single axis knee: less moving parts, simple design, lower fabrication costs, lighter weight, less stable at heel strike, one axis to absorb gait stress
Polycentric-inherent stability at heel strike, initiate swing easier, heavier, increased maintenance, the pivot pt is further posterior and proximal with plumb line in same spot=more stable
Manual lock knee-transfer and limited walking, no buckle when you fall, F1/2, easily femur fracture bc non flexing knee while standing and ambulating, transfer prosthesis or limited walking on level surfaces, simple design, pt must manually unlock to sit
Friction knee- -only effects swing not stance, springs help with knee extension assist, F1/2, mainly transfer prosthesis, limited on level ground walking, acts like a simple door hinge, only one walking speed, friction plates wear and require maintenance
Hydraulic knee-F3/4, resists flexion/extension during swing phase, variable cadence, can change walking speed, heavier due to fluid in cylinder, regular maintenance
Stance Control knee-safety knee, built in breaking mechanism to lock knee during stance, screw prevents open area from collapsing during walking, tighten for heavier patients-*acts like eccentric contraction of knee, F1,2 and 3, added stability for mis-steps and uneven surface, most common in USA, break will wear and knee will fail w/out proper adjustment
Hydraulic swing and stance knee: F3/4, resistance to flexion/extension in swing/stance phase, stumble recovery, ability to walk down stairs and ramps, heavy due to fluid and maintenance
Microprocessor swing- F3/4, provides resistance to flexion/extension during swing, variable cadence, on board microprocessor analyzes gait and selects resistance for smooth swing, stance phase control is more important, so this knee is not as important bc it only controls swing phase, added expense due to tech, maintenance is essential
Microprocessor swing/stance: F3/4 sometimes 2 if require added stability, analyzes gait
50X/second in order to adjust for every step and movement
Microprocessor controlled knee-provide comfort, stability, function and freedom o Gold standard-ensures the knee is always in the most stable and appropriate adjustment, ultimate stumble recovery and stability o How do they work: on board comp to analyze gait 50 per second, sensor at knee to tell you what position it’s in (flexion/extension angles), and at ankle to tell you if there is pressure on the heel or the toe or where it is, continuous hydraulic adjustment for stability, security and efficient swing and stance, stance is engaged/disengaged as necessary, has lithium battery ion recharger o Transfemoral amputees-will let you go down steps and will catch you if you stumble, so that people don’ t have to think about where they are walking all of the time o C leg-flexes at heel strike, pressure at toe tells knee to unlock and swing freely, c. Describe selection of prosthetic components in terms of Medicare‐established functional levels.
Foot:
FL0-no ability to ambulate or transfer
F1-ability/potential to ambulate/transfer on even surfaces at a fixed cadence
F2-ability/potential to ambulate, and traverse low level barriers
F3-ability/potential to ambulate with variable cadence
F4-ability/potential to ambulate and exceed basic skills (children)
21. Ortho Pediatrics a. Recognize general sequence of prenatal development as it relates to abnormal growth.
Birth-2: most rapid growth, “normal” variations, pes planus, in/out toeing, genu varus/valgus
2-adolescents: ½ of adult height by 2, ¾ by age 9, UE growth before LE, foot grows before rest of LE, trunk grows more in children and LE more in adolescents
Puberty-skeletal maturity: common time for scoliosis and slipped capital femoral epiphysis, psych factors are higher priority like fitting in with peers and visible deformities that alter gait b. Provide examples of growth factors: mechanical, endocrine, nutrition, and metabolic
Abnormal growth: musculoskeletal are 1/3 of all congenital defects, 50% are dev hip dysplagia or club feet
Environment: too big baby, not enough room
Nutrition
Infection
Trauma-during birth, malunion or growth plate deformities-fall/rickets
Neuromuscular-muscle imbalance, secondary to spasticity, CP (stroke b4, during or after birth)-not diagnosed until age 3 bc can’t see changes in brain until then
Metabolic: rickets induced osteopenia and bowing of long bones
Iatrogenic-cradle boards and DDH-so much cartilage in acetabulum, it needs to be shaped to develop correctly
History-birth (term, late, c-section, vaginal), , ventilator, APGAR scores, is there a reason they weren’t as healthy at birth, milestones, family history and parent intuition (they know the child better than you do)
Deformities: pes planus, genu valgum, rotation-most will outgrow over time, but congenital and neuromuscular probably won’t get better (tone or altered posture)
Altered function-due to pain or weakness, older kids will report pain but younger kids will try to compensate, but they won’t report it if it’s not there
Toe walking=CP, gower’s sign=Duchenne’s MD sometimes Becker’s
Pain-sometimes growing pains or sprain/tear, but if unsure and they have nagging pain that doesn’t go away=cancer
MMT-not appropriate under age of 5 c. Describe the mechanism of injury, risk factors, physical limitations, medical and PT interventions for the following:
Club Foot (Talipes Equinovarus)-1/800 births, 10% hereditary o Fetal positioning-mild, serial cast w/weekly progression to change stretch until it is in normal positioning o Neuromuscular diagnosis-severe, surgical correction at 4-6mos, will be tight and they will miss some milestones, night splint, PT-PROM, strength and gross motor concerns
Developmental hip dysplasia-female, first born, hereditary due to small women having large babies or mechanical (positional), cultural or increased incidence w/torticollis o Classifications: normal, subluxtable, dislocatable, subluxed, dislocated o Tests: barlows or ortalanis, galezzi sign, or asymmetry of thigh folds o Treatment: before 3 mos=splint w/pavlik, 24hr wear o 6-12mos=closed reduction then spica cast o Older=muscles release and proximal femoral osteotomy and spica o PT=teach how to walk in cast, then gait train when they get out, PROM and strength
Congenital Muscular Torticollis-shortened SCM, lateral flexion to short side and opposite rotation, facial asymmetry and plagiocephaly o MOI: intrauterine positioning, delivery trauma, post-birth positioning o PT: rule out vision deficits o Botox/surgery: >12mos old, doesn’t respond to PT
Legg‐Calve Perthes Disease (self‐limiting AVN)-20% bilateral, boys 3-13 o MOI: trauma, vascular anomalies, infection, thrombic incidents o s/s: pain in groin, knee and thigh, loss of IR, abduction and hip extension, antalgic and trendelemburg gait o 4 stages: condensation (necrotic femoral head), fragmentation (necrotic frag absorbed, revascularization, flattening of acetabulum), reossification with vascular supply, remodeling at acetabulum o PT: gait training w/limited WBing, weak core, tight leg muscles, assistive device, varus osteotomy if it goes later in life, PROM, strengthening to support, activity modification and compliance o <6 years: decrease pain, 6-8: casting and orthotics, 9: surgery
Slipped Capital Femoral Epiphysis (femoral epiphysis displacement‐obesity)-displacement of normal position of femoral neck o MOI: rapid growth, trauma, obesity, males, African Americans, at puberty, 22% bilateral
o S/S: pain in medial thigh, groin and knee, antalgic gait, decreased WBing, limited IR, adduction and flexion, ER w/attempts at flexion (captain morgan pose) o Acute-sudden onset, pain <3 weeks, chronic-gradual onset, pain >3 weeks, acute or chronic >3 weeks with sudden exacerbation o Grades: I-up to 1/3 width of neck, II-1/3 to ½ width of neck, III-> ½ width, with grade III there is no passive conservative management they need surgery ASAP to preserve vascular supply o Surgery: stabilize growth plate o PT: gait train w/assistive device after surgery, NWBing, progress as ordered, strength and PROM with focus on core stability
Blount’s Disease (tibia vara‐obesity)-medial proximal tibia involves epiphysis, plate and metaphysic secondary to asymmetric compression and shear forces, present bow-legged o Types: infantile <3 years, juvenile 4-10 years, adolescent 11 or older o Infantile-toddlers, obese or early walker, normal genu varum will improve but blount’s will progress o Juvenile and adolescent: rule out growth plate fractures and infection o Radiographs: sharp varus angulation of metaphysic, wedging of medial epiphysis, widen growth plate, beakening of medial tibial metaphysic with cartilage islands o Surgery: <3 years, HKAFO 23hrs/day, gradual valgus force progression every 2mos,
3-5 tibial osteotomy, >5 yo, osteotomy with lateral physeal arrest and external fixation o PT: gait training w/restricted WBing, strength and range pre/post op, external fixator management
Pediatric fractures: more avulsion bc ligaments are stronger than bone, bending fractures, increased remodeling (mal and non-union are rare), 2-3 weeks to heal for infants, 4 wk for pre-school, 6wk for 7-10, and 8-10 wk for adolescents
Rotational deformities: in/out toeing from ante/retroverted hip or tight IR/ER, could come from tibia/femur or both, craig’s test or thigh foot angle, look for symmetry, muscular can be treated, bony can’t
Amputation: UE fit when they begin bilateral hand gestures, LE-when they begin WBing, growth may cause bone spikes
Standard orthopedic concerns: Osgood schlatter’s, sinding Larson johanssen, ACL, OCD, patella-femoral , sprains and strains
Sport related-pitch counts, overuse, overtraining