MSK Test 3: LE

d. Pott's fracture dislocation = Fracture + Dislocation

Any dislocation and fracture of malleoli

Collateral Ligament (MCL/LCL) Treatment

Acute SOC (regardless of grade) : 1. PRICE - Compression bandage with ice & leg elevated to decrease inflammation and protect the joint 2. Bracing - Prevent stresses to that side of knee - avoid any valgus/varus stresses (depending on which lig) Overal PT Focus: *Providing STABILITY* to injured side *1. External Support* may be needed at beginning *2. Dynamic Muscular Control* should be worked on with progression of healing -Can not control the knee at the knee -Hip impairments and Foot/ankle impairments - any tight mm. 3. Grades I and II if MCL involved and effusion is present due to meniscus 4. Grade 3 Treatment = Surgery to repair damaged ligament Keep in mind: MCL attachments to Med meniscus & SM to medial meniscus

*Osgood Schlatter's disease* -MANAGEMENT (not really "Treatment)

Again, its self-limiting so treatment would be: INITIALLY: 1. *Educate* pt. about problem & *activity modification*; if they don't decrease activity they could get an avulsion fx -we want to decrease the load! 2. *Long term bracing* to decrease stress/pressure directly on tibial tuberosity; strap should be above tender spot to disperse forces EVENTUALLY (after 4 phases) 1. Work on surrounding impairments i.e. tight joint cap, weak quads etc.

1. describe the mechanism of injury, symptoms, clinical findings and management for i. anterior talofibular ligament sprain

Anatomy: Lateral Malleouls to talus; Angled ant/med. 1. Prevents Talus anterior displacement/inversion/IR 2. *Most common* -weakest; a) Lateral side stressed/loaded more as we come down b) More inversion - lateral ligaments are stressed more 3. MOI: *Plantarflexion & inversion* Findings: -*Extracapsular*-blends with joint capsule (so is CFL); you could have joint effusion under PROM A

c. *Tears of the menisci* -Posterior and Anterior Horn Tears - PERIPHERY

"Horn Tears" = Tears of the tips of the menisci that are attached to tibia *Posterior and Anterior Horn Tears:* @ Periphery: -Better healing response due to blood supply -May respond better to therapy and may not have to get surgery

HIP 1

.

HIP 2 - did not listen to!

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c. *Tears of the menisci* -Bucket Handle Tear - CENTRAL

*Bucket handle Tears*: Central/body -may NOT heal well/respond well because no blood circulation here -may need surgery

e. *Patellar Tendonitis/osis* -Physical Exam & Management

*Hx:* Pain with activities like jumping, squatting, kneeling; pain usually disappears with rest and returns with activity (normal for tendonopathy) *PFC:* inflammation if itis *AROM* - painful for mm action *PROM C* - may be positive opposite for mm action; but think of it as 2 joint mm; so may have negative findings since it wouldn't be stretched at both places for prom C *PROM A* - unremarkable *MSTT* - strong and painful for action *MLT* - positive for opposite mm action *MMT* - defer *ST- Thomas test* (rec. fem.); all may have normal length but should have pain with the lengthening the mm- MLT; but having a tight mm is a different TSI *PFT *- pain at insertion site Management- (Kinetic chain as well) -Regular tendinopathy;

Phase 1: Early Phase of Necrosis -Radiograph

-"Silent phase": unremarkable on plain film radiograph because theres not enough bone to show that progression; no change in joint space or anything that would suggest weird alignment etc.

Total Hip Replacement - General

-Average pt. age = 66 (female) 63 (men) -Females have more THR than males; Why? Ppt says Q-angle but bormann in class didn't really think so -Relieve pain, improve function = Modest activity participation If treating (someone with DJD?) 4-6 and if not getting better then send them to get THR; needs to be optimal age if too early i.e. 50 - chance of having to get another is high; avoid them in young pt.

c. *Pes Anserinus Tendonitis/osis - SarGT* -What does the PA tendon help with?

-Helps with preventing abnormal ER, ABD, and anterior displacement of tibia on femur; -Reinforces MCL, ACL, and posteromedial capsule;

c. Anterior fracture-dislocation of the hip

-Less common Etiology: -Forced Ext, ABD, and ER (opposite posterior)

Meniscus Anatomy: Pic of Slide -What attaches to each?

-Wedges of fibrocartilage; 1. Lateral is smaller and medial is bigger because they match up to the size of the condyles 2. Peripheral - vascular via genicular A; Central - avascular *Functions:* 1. Aid joint lubrication & distribute forces 2. stability 3. shock DISTRIBUTION - not absorbers, decrease friction Lec: Menisci help with stability by making the sockets deeper - "be prepared for exam"

MRI risks (3)

1) Surgical clips can be displaced i.e. brain aneurysms 2) Orthopedic hardware causes image distortion -generally is not a health hazard 3) Pacemakers may malfunction 4) Claustrophobia can also be a factor

Acute/Traumatic Compartment Syndrome -Tx?

1) *Acute* = i.e. kick a ball hits anterior tib resulting in hematoma/swelling (swelling has no where to go) and ends up compressing everything in anterior compartment; if youdont release pressure = necrosis of everything in compartment; 2) *Tx = medical emergency* - need to relieve pressure -have a device that measures amount of pressure and determines if you need fasciotomy or not

Structural causes for PFPS?

1. Small lateral condyle & more prominate medial condyle; usually patella stays between groves but if you have smaller lateral condyle = pressure won't go on medial side but will go on lateral side = more lateral drifting of patella Over time? Patellofemoral joint will degenerate and become chondromalacia patella. 2. Patella Alta - high riding patella = abnormal tracking 3. Genu Valgum - abnormal biomechanics Cant change if they are born with it - just work on surrounding tissues by strengthening/stretching

Phase 2: Revascularization -Pathogenesis -Symptoms?

1. Dead epiphysis becomes revascularized -body responds to cell death by sending new collateral vessels to the area where more bone tissue will be laid down Problem? 2. "Biological Plasticity"- the new bone cells are soft and moldable and fibrotic - weaker and pliable - different quality - could result in mal aligned head its fragile, would not tolerate normal forces that normal bone could; 3 "Pathological Fracture" -Symptoms: 1. Pain - may say it hurts anterior and deep toward groin (ST: FABER/Patricks - general hip pathology) 2. Limping - give them an AD to take weight off Lec: What things could you do? swimming is good to keep moving etc without the loading

a. define osteochondrosis.

1. Developmental derangement of normal bone growth, mainly involving epiphyses -as you grow the epipheyes grows in a mal-fashion 2. Self-limiting -very disabling for people but it will stop on its own but your left with a joint that is severely disabled Femur is smaller and lots of effusion as you can see by the picture

Total Knee Arthroplasty: Components

1. Femoral: Cobalt-Chrome metal, cemented into femur 2. Tibial: Chrome or titanium with plastic tibial insert for tibial condyle 3. Patella: Plastic cap/cup; surgeon can set pt. ROM because not one-size fits all - thats why you need to make sure you talk to surgeon *These components FIT SO WELL together that it would be harder to just use 1 of the components; so usually all 3 are needed *no attachment for cruciate ligs; ACL always cut sometimes PCL can be spared

Fx of the Shaft = e. transverse, oblique, spiral fractures of tibia i. stable. ii. unstable.

1. Transverse (left) 2. Oblique (top right) 3. Spiral (bottom right) Tibia is one of biggest WB bones (after femur) so these are 1. Slow healing and hard to rehab because person is still going to bear some weight on it - you can't ask someone not to walk at all/completely immobilize; 2. Tx focuses on the surrounding impairments - strengthen weak mm, loss of mobility, swelling, edema, etc.

PCL intact vs. torn

first 6-8 weeks no HS exercises

"Important slide" - no connections

74 - popletius attachment (on lateral fem cone) inside dotted like aka capsule - intracapsular - can have effusion 75 - gastroc = outside dotted line = no effusion ACL/PCL - outside but exception is anteromedial fibers

What are the ABCs?

A:Alignment B:Bone density C:Cartilage space S:soft tissue

Ankle Sprain Sequence - Lateral Side

ATFL, anterolat capsule, distal tib-fib lig, CFL, PTFL PTFL and Deltoid ligs - rare

g. describe the difference between anterior approach total hip replacement, posterior approach and minimally invasive total hip replacement in terms of post-operative rehabilitation, patient education, and outcomes

Anterior Approach: Dislocate hip anteriorly -Surgery position & precautions same = -Extension, ER, ABD -Advantages to anterior? 1. Most of the times older people don't want to put their legs in these positions - less likelihood of dislocation; 2. Don't cut through the glutes and create weakness like posterolateral does 3. Minimal inscision -Challenges? Femoral artery/vascualr structures - harder approach surgery wise Posteriolateral Appraoch: Dislocate hip in posterior direction via glute max -most common -Surgery position & precautions typical: Flex past 90, excessive ADD or IR - this could dislocate the new hip Disadvantage: 1. Cut through glut max causing weakness in glutes and pain later on - these pt. may be (+) for trundelenburg Outcome Considerations:

General MCL

Attachment: medial epicondyle to shaft of tibia -Also attaches to medial meniscus and joint capsule -So, PROM A you could have joint effusion because of blending of fibers Taught in full extension and ER of tibia Restrains excessive Valgus/Abd force Prevents anterior displacement of tibia on femur VPP: ACL/PCL = Internal joint cap = Taut in tibial IR MCL/LCL = External to joint cap = Taut in tibial ER

Voice over info about dynamic & static stability of the knee

Because of the big femoral condyles on the tibia, there is great importance of having stability from the ligaments/tendons/menisi etc; Statically our knee is stabilized by the joint capsule, menisci and the ligaments Dynamically it is stabilized by tendons from the quads, hamstrings, popliteus, gastroc, gracillis, IT band, sartorious

For viewing CT:

Bone is white Muscle is gray Fat is dark Air is black *Modality of choice for viewing bone *Best modality for evaluating of loose bodies/subtle complex fractures

4. compare and contrast the characteristics and use of plain film radiograph/CT/MRI/US

CT: Best modality or evaluating of loose bodies/subtle complex fractures; outline of bone is very bright; uses radiograph MRI: Superior method for viewing soft tissue detail and certain pathologies of bone; some risks associated; Uses magnets US: has to have very low radiation - i.e. we think about kids with it; based on tissues different reflective properties

Plantar Fascitis - Causes -Abnormal biomechanics -Contractile -Non-contractile -kinetic chain

Causes - Plantar Fascitis IS A TSI Many reasons for excessive stress on fascia; we need to find the reason and fix it *Abnormal biomechanics* *1.Excessive hind foot Pronation* = PF on stretch -most common; i.e. rearfoot in eversion and DF and cal cation is away and laterally - stretches it *2.Excessive Supination* = PF on laxity -i.e. more ridged foot and higher arch creating more stress on fascia - it can't relax and conform to the ground *Contractile* *3. Muscle Imbalances* -tight/weak mm *Non-contractile* *4. Excessive Ligament/Capsule Laxity* - can stress the fascia leading to fascitis or osis *5. Excessive Capsule Tightness* - resulting in abnormal biomechanics of foot as they are walking *Kinetic Chain*- i.e. could be genu valgum or weakness in a hip mm thats causing the over pronation/supination etc.

Plantar Fascitis - Clinical Findings & Best Steps

Clinical Findings-PFT, Great toe DF -Hx = usually gradually and cause unknown; pain under heel that increases with weight/in the morning -PFC - -AROM - usually full -PROM C - pain under great toe during extension with overpressure -MMT - weak foot intrinsics Best steps? 1. PFT - over insertion over calcaneous 2. ST - Windlass test - lengthening PF by doing DF with Great toe DF and have pain in heal area

6. Patella Dislocation: a. describe the mechanism of injury, symptoms, and signs of patella dislocation versus subluxation.

Compared to subluxation 1. Subluxation - Patella slides back into normal position spontaneously Medical management - if dislocated? 1. Closed reduction with knee extended 2. External Support -you would treat the tightness after Treat subluxation - stabilize, dynamic control, ABD ER, look at quad-ham ratio/co-contraction, its mainly the imbalance between those - Closed chain activities

7. define the structural deformities of: a. anteversion b. retroversion

Coxa Vara & Valga = in Frontal Plane Anteversion & Retroversion = in Transverse Plane

Lateral (Tailor's) bunion

Happens on lateral side of 5th MTP - Same type of rotation occurs -Similar to bunion at fist MTP -Articulation is with 5th met and cuboid -people with excessive pronated rear foot and mid-foot

c. *Tears of the menisci*

Depends on if tear is at periphery or body; why? because healing time and treatment response! 1. Bucket Handle Tear - CENTRAL 2. Posterior and Anterior Horn Tears - PERIPHERY

3. describe the cause of *quadriceps inhibition, and effects of knee effusion*, according to Spencer et al.

Don't nee do read article; just know findings What were Spencer et al results? -Joint effusion shuts down surrounding muscles, decreases their firing patterns and strength to protect the joint; -Quads shut down 1st then the glutes; Take home message: Clinically, treat the *effusion/swelling before strengthening*! You can't tell if body is responding to effusion and shutting down that mm or if its actually weak

b) hallux valgus = position of toe deviating laterally -Etiology

Etiology 1) Hypomobility- Hallux rigidus 2) Hypermobility- 1st TMT, MTP -Usually problem above the kinetic chain = *Laxity at TMT resulting in rotation at 1st TMT joint (base of met with medial cuneiform)* *-1) Excessive FF pronation* = the dorsum/top of the first MTP can rotate medially - creates a twisting down MTP joint creating a lateral deviation and HV at MTP *-2) Excessive FF supination* at TMT - MTP will follow least resistance and you'll have lateral deviation still ??? confusing 3) Joint effusion 4) Edema 5) Muscle imbalances Keep in mind: Osteokinematic movements = in relation to middle to i.e. big toe is in excessive ADD (more toward middle toe) Arthrokinematically = in realtion to body midline i.e. big toe is in excessive lateral deviation

3. discuss the etiology, evaluation findings and treatment for: a. trochanteric bursitis -Etiology & Exam

Etiology: -Trama to one of the bursae? i.e. fall -More likely Overuse of abnormal biomechanics Exam: 1. Pain - depends on SOC 2. Hx - may roll on it during sleeping and have pain (different than "night pain" that would just wake you up), maybe pain with stairs/prolonged walking 3. PFC - generally won't be able to find much because its so deep 4. AROM - Normal range but pain with active Ext and ER - glute max (which is on top of it) contracts; 5. PRROM - Normal range but pain with end-range ADD/IR/Flex 6. MSTT - False positive b/c not tendonitis: Pain with ER, EXT (and ABD?) 7. MLT - deferred due to MSTT 8. PFT - "Lateral hip pain"

3. Discuss the etiology, examination findings and medical/physical therapy treatment for: a. hip labral tears

Etiology: -Trauma/athletic injury -Instability -Developmental dysplasia -Impingement -Degeneration Exam: -General Clicking, Popping, Locking (labrum is fibrocart) 1. Pain - anterior hip/groin 2. PROM C - Rotation is limited 3. Anterior/Posterior Hip Labral Tear - ST Treatment: -Conservative and Surgical

Hallux Valgus & Medial Bunion

Excessive pressure in this area body creates bursa to protect bony outgrowth and reduce friction = presents as bunion; There is excestosis and callus formation Treatment - shoes with wider shoe box or toe spacers between 1st and 2nd toes - can help maintain normal alignment -remember to look above the chain - it may be problem at TMT causing it so you'd need to fix the cause Surgery - injections or bunionectomy

b. fractures of the femoral neck

Femoral Neck = INTRA Capsular -Torsional forces -Most problematic of all fx - AVN Clinical Features: No obvious swelling (bc inside joint) Radiograph: 95% are displaced (duh, its the neck) Treatment: ORIF or Hemiarthroplasty Outcomes: AVN, Non-Union, DJD

3. describe the clinical exam findings for a capsular pattern restriction at the knee and apply to a clinical case.

Flexion limited more than Extension (both limited though)

What are the hallmark findings of DJD? What kind of Treatment

Hallmark examination findings -Gradual onset -Stiffness -Weight bearing pain -Compression pain Treatment Conservative-catch early Surgical Voice over: No sudden injury, stiff in moring because not normal movement of fluid in joint but as they get up and moving they have less stiffness (increased fluid into joint); rule out any tendon problems in the area before you say its djd ST to load/compress joint and if they have pain you can think more cartilage probs Prognosis better if you can't early and treat them well so they don't have to take meds/have hip replacement; want to correct biomechanics issues

Discuss the total knee replacement surgical procedure in regard to: a. indications

If pain is bad enough to influence their function -Goal of surgery is to Relieve pain, improve function = Modest Activity participation Pain can be from: 1. Joint degeneration / osteoarthrosis 2. Primary/Secondary 3. Rheumatoid Arthritis 4. Ligamentous Instability 5. Infection 6. Avascular Necrosis

TKA Complications = no volume

Infection Deep vein thrombosis Pulmonary Embolism Patellofemoral joint usually limited Thrombosis = stays there; Embolism - its traveling in blood - good get to lungs and you could die 2 big first 2 DVT = pulmonary emoblism = death PFT altered after surgery - getting patellar mobility is huge - need to get patellar mobility back using manipulations

5. utilizing hip/pelvis anatomy, biomechanics and bone pathology explain the statement, "the fracture is the cause of the fall rather than the result of it".

Lec: "Sometimes The fracture is the cause of the fall rather than the result of it" - fall bc fracture is there

Osgood Schlatter's disease -Picture

Left you can see the residual deformity and on the right you can see avulsion fx on radiograph

5. identify anatomical landmarks given standard radiographs and/or MRI

Look at imaging pics - Images will be on test according to tutoring notes

e. "unhappy triad"

MCL, ACL, Medial Meniscus

b. tendo Achilles rupture. MOI (2) Other? (4)

MOI 1) *Pushing off (i.e. during sports) with knee extended* -Tennis,raquet ball - quick short burst movements pushing off really quick spontaneous 2) *Sudden passive DF with resisted PF that could happen with jumping/falling* Other: *1) Avulsion Fx of calcaneous* common; -Usually they may have some underlying tendonopathy going on or it is weak already? *2) With a full/complete tear* -pt. will tell you it sounded like a loud pop and the achilles rolls up into calf (due to large gastroc) *3) If exposed to Cortisone injections* in area? -more prone because tissue is more brittle and decrease integrity of collagen = increase chance for rupture 4) One of thickest/strongest tendons in body with no synovial sheath

MRI of meniscus

MRI T1 because the fat is bright; You can see at arrow the black wedge is meniscus and white fuzziness = fluid or break in meniscus

IT Band Friction Syndrome -Management

Management: Treeat like any tendonopathy -Decrease stress on lateral aspect on knee -Could do bracing, tape area to decrease stress, ST manipulation of mm that attach; you can stretch any tight mm; strengthen weak mm above or below to decrease stress at knee; Lec: Syndrome - lots of things could be going on; Treat what you find!

1. identify the difference between: a. capsular pattern as described by Cyriax b. capsular pattern as described by Kaltenborn

Most Restricted - Least Restricted Cyriax: FAME - Flexion; ABD; MR, Ext, LR Kaltenborn: MEAF - MR, Ext, ABD, Flex, LR Lec: *KNOW THESE*

2.describe the etiology, signs and symptoms, and PT management of the following: a) hallux rigidus = loss of motion at toe -General

Most extreme case of loss of mobility like OA of the first met; degenerative changes in joint and it fuses - way worse than tight jc; there is fibrosis and complete loss of mobility On radiograph: -less joint space, cartilage is degenerated, bone on bone, may see osteophytes or bone spurs

More on Soft Tissue Restrictions causing PFPS - STOPPED HERE

Most people think weak medial muscles and tightness of lateral side; Lec: people have more problem in CC; in CC whats moving? the femur! we should focus on mm that are moving/controlling the hip; its really the femur that is IR; Reasons for IR of femur? weak ER, ABD - Glutes & Abdominals/Core = causing Anterior tilt; and tight ADDs/IRs -Strengthen ER, ABDs and Core mm These people present with genu valgum; so strengthening VMO would pull them more that way - also you can't isolate VMO

Menisci Biomechanics VPP -Which has more mobility and how is this relevant in terms of injury?

Move in direction of femur movement! CC: where ever femur moves = menisci in same direction (i.e. flexion they move back, then back to neutral they move forward) *Mobility* 1. Medial menisci is 2x LESS mobile than lateral because more structures attach to it that anchor it down; 2. MM = less mobility = can't get out of the way during movement = higher risk of TEAR/INJURY 3. LM = more mobility = able to get out of the way

Treatment - Non-Operative

Non-Operative: Depends on if injury to body or periphery 1. PRICE modalities to decrease pain; we want to maintain ROM at knee and work on strength & endurace 2. *Keep in mind for MM - semimem attached; don't start HS strengthening too early! Goals: work on motion, improve WB, & help with mobility inside joint cap (the effusion usually present can lead to decreed mobility); can usually return to sport in 4-6 months

c. osteochondral lesion

Onset: Exam: -Compression, weight bearing, limited PROM C, Impingement signs

b. pre-surgical status c. performance of the procedure d. post-operative rehabilitation e. complications and outcomes

Performance: During the procedure the surgeon flushes fluid into the knee to be able to see whats going on; this is why after surgery you have a lot of effusion; in the pic the white bag is a catheter into knee aka drain - it flushes fluid out; if you see these on your pt. don't pull on them

7. Plica: a. describe the symptoms and signs of symptomatic plica.

Pathology 1. Excess synovial fold not reabsorbed with development growth 2. Most Common-Medial patellar plica; - Anteromedial? Suprapatellar also common Lec: what is plica? as we develop we grow into different compartments that are lined with synovial; i think plica is when it doesnt go away like usual?

b. describe the medical management options for patella dislocation.

Pathology Excess synovial fold not reabsorbed with development growth

*Pes Anserinus Tendonitis/osis - SarGT* -Physical Exam Findings

Physical Exam 1. *PFC:* Swelling; if inflammation also present -itis *2. PROM C:* Positive when you stretch them; (+) opposite the mm action; may get negative findings because you may be stretching through 1 joint; would see more positive findings during MLT where you're stretching them over 2 joints; End-feel = abnormal muscle *3. PROM A:* unremarkable - outside jc *4. MLT:* same as PROM C; opposite the mm actions but remember they are 2 joint mm so need to stretch them at hip and knee!; range would be normal but pain *5. MSTT:* Strong & Painful SarGT actions: Knee Flexion & IR (ALL), Hip Flexion (Sart) & Hip Ext (ST), Hip ABD (Sart) & Hip ADD (G); if MSTT is negative it may be just because hip is strong *6. PFT:* tenderness at PA tendon; depth depending on TR One particular ms involvement? - MSTT; if only 1 mm only treat that mm Note: for PROM C you don't test tibial ER/IR but you can MSTT actions at the hip that would help - i think true for popliteus & SM tendonopathies too

TKA Considerations = no volume

Quadriceps Weakness Why? mainly bc surgeon makes incision in mm, or trauma surgery or immobilization - need to strengthen during rehab Restricted Range of Motion Why? trauma sur, effusion, swelling Continuous passive motion machine Is it useful? No long term no difference, lots of compensations at hips and back What variables predict post operative knee range of motion? ROM before is a big factor in gaining ROM post op Poor ROM prior = poor ROM post surgery

Rotation of 1st Met ray at TMT joint

Sesamoid bones under 1st MTP have moved laterally (sesamoid bones are pulley for FH tendons) - MTP becomes incongruent and sesamoid bones are present laterally - this rotation causes the medial part of the Met head to be more prominent Weight bearing could shift from the 1st met head to the 2nd or third Body protects this medial prominence with bunion

ACL -Clinical Appearance/Exam

Signs & Symptoms form AROM, PROM etc. all that - depend on Grades (already talked about)! PROM A: Anteromedial fibers of ACL blend with joint cap; so you may have joint effusion (she says this a million times) PROM C: Extension usually limited, flexion could be due to swelling/pain; Amount will depend on the grade ST: Special tests- Ant. Drawer, Lachman, lat. Pivot shift -Lachman the best one -TR will come from Special Tests - PROM A may also stress it but to do it maximally you want ST

Other locations? - spine, elbow, foot, heel (all called different things, listen to PPT)

Spine = Shermans disease Hip = Leg-Calf Navicular in foot = coolers Elbow (cap) = Panners Calcaneous = severs disease Keinbocks Ostercslhtek

What is harder to rehab a fracture or a sprain?

Sprains: 1. Take longer to heal - less BS compared to bone 2. People get less medical help 3. Cant strengthen them - particularly ankle because there's not a lot of musculature around the joint 4. Collagen is never as strong as original - reason for CAI Better to break a bone than a bad sprain!

Structural vs. Functional Hallux Valgus

Structural (ridged) = valgus positon will not be able to be changed; you cannot correct the alignment - changes within the articular surfaces - interventions will not help Functional (mobile) = you can correct the alignment

2. compare and contrast the symptoms, signs, and clinical management of -*Synovitis vs Hemarthrosis* of the knee

THIS CAN BE APPLIED FOR ANY JOINT IN THE BODY (We just cover it in knee section) Both = intra-capsular, both have some sort of fluid aka effusion in the capsule (one is blood and one is synovium) What are the clinical features of each? *Synovitis:* 1. *Gradual onset* of effusion, uncomfortable 2. PFC: warm joint 3. PROM A: swelling end-feel (will still be painful but you will be able to have positive findings for PROM A; it is not as reactive as HA). *Hemarthrosis:* 1. *Rapid onset* of blood (effusion) in the joint & severe pain 2. PFC: hot joint 3. PROM A: difficult to obtain end-feel because reactivity is too high *What can cause synovitis?* Injury to an intra-articular structure (the inner layer is what secretes the excess fluid) maybe over-stretching it etc. -Tx: *PRICE and activity mod*; Grade I and II glides/Distraction *What can cause hemarthrosis?* -Severe damage or trauma resulting in tearing of the structures and bleeding of capsule -Tx: Medical Emergency! Blood in capsule will eat at cartilage, need to *send them to doc immediately for aspiration then PRICE principle* basically treat hemoarthrosis as synovitis after medical treatment; but make sure you monitor the warmth/temperature

Etiology of IT Band Friction Syndrome -Possible TSIs leading to the Friction

TSIs that can lead to ITB friction: Think kinetic chain; 1. History of trochanteric bursitis/bursosis 2. Leg Length Discrepancy 3. Hip Musculature imbalance 4. Adhesions of the ITB 5. Tightness of TFL and / or Glut Max, Hams, or Quads. -Usually tightness in lateral compartment 6. Genu Varum -Not a TSI, just note if its a structural cause (GV) or mm imbalances 7. Excessive rearfoot pronation leading to increased internal tibial rotation. -Also not really a TSI - more structural 8. Forefoot Varus 9. Inappropriate shoe wear or running surface such as running on a slanted road.

*Pes Anserinus Tendonitis/osis* -Management

Tendonopathies are usually result of a problem not the cause! TREAT THE BIOMECHANICS Itis - Reduce swelling, inflammation etc. Osis - Reactive or Degeneartive? Reactive: Reduce load & activiy mod Degenerative: Load tendon heavily and work toward eccentric Make sure to look above and below the kinetic chain! - look at hip and foot; Want to decrease VALGUS stresses at the knee

4. describe the clinical features, radiographic features, treatment, and complications for a. trochanteric fractures of the femur

Trochanteric = Extra Capsular Clinical Features: -LE is ER and appears SHORTER -Swelling in surrounding ST Radiograph: Severely comminuted Treatment: ORIF; WBAT within a few weeks Outcomes:

e. describe the difference between a cemented and a non-cemented prosthesis, in terms of how the prosthesis fixes to the femur, and the implications for post- operative rehabilitation. (They are types of THR)

Uncemented: Press Fit -Rough texture; bone tissue grows into rough porous component when inserted into femur -more restrictions /slower healing Cemented: glued around the prosthesis; its a solid fixation; they can get it in the morning and be walking with a cane that afternoon -femur component and ace tabular component is glued around the prosthesis and the surgeon glues to the bone tissue Healing Considerations: -Cemented = You are able to weight bear quicker -Osteoporosis or older age probably want to use cemented

Recent Advances = no volume

Unicompartmental Replacements; only med or lat replaced other sid normal bone and cart i.e. severe genu valgum - medial compartment more wear and tear an flat is still good; Gender specific prosthesis - female is smaller Minimal invasive procedures (smaller incisions) Quad sparing - don't cut quad tendon but take who patella and dislocate to side PCL sparing also Computer assisted procedures

e. *Patellar Tendonitis/osis* -Etiology

VPP: Overuse/overloading of patellar tendon; repetitive squatting, jumping etc. abnormalits in hip or ankle could result in excessive loading in p. tendon; tight joint cap or adhesions flexibility, strength issues -could all lead to excessive stress = tendonopathy Goal - want to catch at itis or reactive oasis - decrease loading to heal; itis- decrease swelling osis - unloading tendon & activity mod - freq, intensity, timing - treating like itis without inflammation osis deg - good load to tendon - eventually eccentric to break cycle Some theories suggest that degenerative tendinosis you have microvascularizaiton - new blood vessels and even nerve endings are in the tendon - this could cause pain so by loading the tendon your trying to break the vessels/cycle of degeneration so tendon can heal another - as we are loading we are trying to flush out all the NT that are in significant amount in these tendons - were breaking the cycle Overloading/overuse? lecture: running, equating stairs, knee movement flex/ext; rest pain goes down

7. describe and apply Greenspan's elements of fracture description to radiographic images:

a. site and extent of fracture b. complete or incomplete c. alignment of fracture d. direction of fracture line e. special features f. associated abnormalities g. special types

Voice over DJD

mostly happens over time with age; Primary no real reason or cause you can figure out & happens with time, just associated with age; Secondary there are predisposing factors - previous trauma, injuries to joint cap etc. anything throwing off biomechanics of hip joint- you can find a cause Know how it progresses; 2 main reasons for progression 1- tight hip capsule you don't get good unweighing which is necessary for functioning/health of joint - pumping affect to nourish cartilage; cartilage is compressed and no healthy loading; you could have loss of ROM and get focal wear and tear and not uniformly because forces are not distributed throughout surfaces - this will result in wearing down sooner; Stiff joint that does not want to move well 2- muscle weakness - anohter biomechanical factor i.e. weak glutes throws off biomechanics of hip joints and wears down on cartilage quicker - this is were we can help them -slow down progression & restore mobility i.e. joint mobs; also strengthen weak mm & stretch tight mm.

Grades of Ligament Tears How are they different clinically?

What is the difference between each grade? Grade 1: *Minimal tearing* of ligament fibers Grade 2: *Moderate tearing* of ligament fibers Grade 3: *Complete tear* of ligament How do you CLINICALLY tell the difference? *G 1: ST to test integrity - Pain & No Laxity* -Pain during ST that is stressing it - but may or may not be painful at rest -Minimal to no loss of function, no bruising, minimal to no pain, minimal to no swelling if LE pt. can usually ambulate i.e. sprain ankle and we still walk; usually ST are best for TR *G2: ST to test integrity - Pain & Moderate Laxity* -Some loss of function, decrease motion, there will be swelling, and PFT *G3: ST to test integrity - No Pain & Significant Laxity* (Maybe initially some pain due to swelling but eventually no pain) -Total loss of function, inability to bear weight, need AD, increased in motion, diffuse swelling, extreme pain with PFT at beginning then no pain later on Lec: Focus on the different grades, if given a case make sure you include which grade as a TSI

Chronic/Exercise-induced/Exertional Compartment Syndrome -Tx?

(who we will mainly see) 1. Pt. will complain of pressure/pain in lower leg as they run etc. 2. Muscle imbalances = over working of one mm group = low grade swelling/edema = micro trauma to structures = no where to go because of non-elastic fascia = pressure built up in compartment -i.e. weak anterior mm (DFs weak) and gastroc/soleus (PF) tight - mm imbalance causing pre-tibial mm to work to hard = inflammation; fasica can't expand = lots of pressure on nerves; 3. Pt. reports pain goes away with rest but comes back with activity *Treatment* = Find cause - mm imbalance, weakness, tightness, etc

d) Metatarsalgia

*"Metatarsalgia" - pain on met heads, global diagnosis* (anytime pain beneath met head they could have this) *Etiology = anything that causes excessive Pressure* 1. Depressed transverse arches = leading to excessive pressure around heads - think of it as bone bruising or excessive pressure on met heads 2. Standing on long duration or working on concrete = pressure = tenderness/inflammation 3. Could be from bad shoes = excessive pressure *Treatment = take pressure off* -1.) Shoe modification - metatarsal pads - distribute weight evenly; maybe wider shoes -2.) Strengthen eccentric mm

e) Morton's neurom -what is it? what causes it? what kind of symptoms? more common in who? Diff diagnosis with?

*"Neuroma - nerve pathology"* 1. Thickening of tissue around the nerves due to fibrosis -Where the plantar nerves split into interdigital nerves between the met heads the bundles could spontaneously get fibrotic/irritated; problems are between the heads 2. Causes- most of the time unknown; but associated with trauma, could also be autoimmune/genetic, mechanical 3. Tender *between met heads*-2nd and 3rd MT (metatarsalgia was underneath met heads) 4. Nerve symptoms-sensations/tingling/numbness -sharp pain under foot with sensations going into toes when they walk or stand 5. Female: male 9:1 Diff. Diag. with Interdigital nerve entrapment? W/ entrapment - remove pressure & symptoms resolve W/ Mortons neuroma - wouldn't see sympt

d. *Popliteus Tendonitis/osis vs. Semimembranosous* -How can you differentiate?

*1. Attachments:* The Pop only has attachments around the knee; SM attaches to the hip at the ischial tuberosity *2. Actions:* Problems unlocking knee = pop; Problems with hip extension = SM *3. MSTT:* Strong and painful for knee flex and IR and hip ext = SM *4. Swelling:* Pop more swelling lateral knee; SM would be more medially; *5. PFT:* positive on lateral for pop; medial for SM and also at the hip 6. Pop mimics PCL pt. may have pain with downhil running walking but not uphill; SM mimics Medial meniscus injury

Tendo Achilles rupture -Clinical Findings

*1. PFC* -Complete Tear = you'd feel a complete gap; and even in SI you may see the tendon is not intact; in left heel you can see the tendon is absent and it's rolled up so as you palpate proximally you could feel budge *2. AROM* -CT = no PF because of full tear *3. PROM C* -CT = excessive DF (depending on swelling - you'll for sure see it in later stages) *4. Special Tests-Thompson* -Thompson (+) *5. Movement analysis* -Pt. have no push off at all, they won't be able to walk properly and they have no active DF *6. MSTT* -CT = Weak and painless for PF - you would not defer MLT or MMT *7. MLT* -CT = excessive length with DF; *8. MMT* -CT = zero strength for PF

Autografts: Patellar Graft Vs. Hamstring Graft for treating a torn ACL?

*1. Patellar Graft:* -Preferred because easy to get to -Heals fast -Holds well in its location DRAWBACK = pain at front of knee after surgery; pt. may have problems kneeling *2. Hamstring Graft* -Take ST tendon (sometimes Gracilis) and arrange it in strips and sutured together Why would a surgeon prefer this method? - NO PAIN at front of knee and NO PROBLEMS KNEELING Overall Outcome = NO MAJOR DIFFERENCES major differences; strength and stability are good after both; but with HS no pain or problems with kneeling

f. Tibial Plateau Fracture -Etiology & Treatment

*Etiology* - older people with weak bones 1. Crushing injury to lateral aspect of knee with foot on ground, creating a Valgus force -Drives the tibial plateu into the condyles 2. *Valgus force in older population* -Typically valgus force would create MCL injury but older people have such weak bones that they often have an avulsion fx and part of the tibia is pulled away 3. Blunt force trauma *Treatment* -Usually comminuted (more than 2 boney frags) usually have HA because blunt trauam- injury to other structures; Tx depends on damage - ORIF or External Fix with closed reduction

4. name impairments and tissue specific impairments that may be a source of anterior knee pain. Note these are not TSIs yet

*1. Rotary limb mal-alignment* -misaligned LE; i.e. Rotation of tibia on femur - could be from weakness at hip at G. max or med or tightness could cause excessive ADD = Genu Valgus = Strain on knee = medial aspect = joint laxity; any mm imbalance leading to Genu Valgus that could lead to excessive stress on knee; Moral of the story = check above and below knee for problems -could be anteversion/retroversion, genu valgum etc. - position *2. Abnormal position of tibia relative to femur* *3. Patellar mal-alignment* *4. Knee hyperextension* -Muscle imbalances - what would be strong/weak causing it = would be your TSI -Also hyper mobility as a cause for PFPS; excessive mobility or laxity = genu valgum at knee = increased lateral mobility of patella = increased Q angle *5. Increased foot pronation* -Excessive rear foot pronation = genu valgus at knee could be causing the stress at knee aka PFPS *6. Abnormal tracking and crepitus in weight-bearing* *7. Soft tissue restrictions* -Hypo mobility = soft tissue around knee is tight = could stress patella more, it doesnt track freely during flex-ext etc. More: tight IT band, tight lateral retinaculum, tight quads; could all be hypo mobility sources leading to PFPS *8. VMO atrophy* *9. Attachment of medial retinaculum* *10. Pelvic instability* -i.e. excessive anterior tilt - obese - weakness in core mm; how that can relate to stresses down chain; excessive Lordosis/Anterior tilt = IR at hip and weak glutes, tight ADD = excess genu valgus = rear pronation = excessive stress on medial side of knee = abnormal tracking of patella/anterior knee pain VPP: Basically look up and down the chain for the TSIs for PFPS Which mm usually get tight/weak in LE? HS, ADD, Gastro = tight; if tight think how they can create stresses on knee Glute, Quads = weak; think how weakness here can result in PFPS These tight/weakness become the TSIs; increase Q angle = genu valgum, femur anteversin, tight lateral retinaculum = stress on patella = abnormal tracking of patella = PFPS

c. uni-, bi-, and tri-malleolar fractures

*1. Unimalleolar* - 1 malleolar fx; either tibia or fibular -Avulsion fxs also something to consider! i.e. ATFL injury can sometimes pull a part of the fibula as well *2. Bimalleolar* - both malleolar fx; *3. Trimalleolar* - Both malleoli + one other structure -1) another piece of tibia or talus, another lig strain, any other mm involved -2) Posterior margin of tibia -3) Talus -4) Soft tissue (lig./muscles etc.) Management - Options 1. Closed Reduction - walking boot or cast 2. ORIF with plates and screws - if highly displaced

Compartments & Contents Anterior (3) Lateral (2) Deep posterior (4)

*Anterior Compartment* 1. Deep peroneal nerve 2. Anterior tibial artery and vein 3. DFs *Lateral Compartment* 1. Superficial peroneal nerve 2. Peroneal mm. *Deep Posterior Compartment* 1. Tibial nerve 2. Posterior tibial artery and vein 3. Peroneal artery and vein 4. Tib post., FDL and FHL (Tom, Dick, Harry) Common one for Deep Posterior Compartment *1. Rear foot pronation* - mm may have to work harder during gait cyle = over working mm = inflammation = pressure on nerves, arteries, veins

*Osgood Schlatter's disease* -Clinical Appearance/Exam Findings

*Clinical Appearance/Exam Findings* 1. Pt. may have visible bump from the bone laid down at spot after they have gone through the 4 phases - bigger tibial tuberosity 2. Pain with QUAD CONTRACTION 3. AROM (FP) - would have pain with contracting quads, but quads are not the problem 4. PROM C (FP) - pain with knee flexion - stretching quads (again, quads not problem) 5. PROM A - unremarkable 6. MSTT (FP) - strong and painful for quad tendon 7. MLT (FP?)- pain with stretching quads - painful thomas test? 8. MA - problems with squatting, running, jumping etc. 9. PFT - tender over the spot/Tibial tuberosity 10. ST - Thomas

*Osgood Schlatter's disease* -Demographic & Differential Diagnosis How is it different than patellar tendonitis/osis?

*Demographic* -Most often Young males; known as "growing pains" usually resolves around 18-19 y/o *Differential Diagnosis = Patellar tendinopathy* -Clinically they present the same, so you would probably start treating them for tendonopathy by applying good load to the tendon -Difference = Patellar tendonopathy would respond to the treatment; OS the pt. would not get better or get worse *How is it different than patellar tendonitis/osis?* 1. Patellar tendonopathy would respond to the treatment of loading the tendon; OS the pt. would not get better or get worse with loading the tendon because its a boney problem 2. Imaging is different - best step to differentiate!

Meniscal Tears -Etiology

*Etiology* 1. As you *compress meniscus* (via squatting or weight wearing) and apply too much of a *rotational force* you can tear the meniscus 2. Associated with activities like squatting, jumping etc. and that have varus and valgus stresses applied -Varus stress during motion = lateral tear -Valgus stress during motion = medial tear (more common) 3. Usually happens on twisting on *semi-flexed knee*; because rotation not possible in extension Higher incidence of injury than lateral meniscus

Tears: ii LCL -Etiology & Signs and Symptoms

*Etiology* 1. Blow to medial knee *Signs and Symptoms* 1st degree sprain -Varus stress *painful with NO increase in mobility* -minimal swelling or loss of function etc. 2nd degree sprain -Varus stress *painful with moderate increase in mobility* -more swelling & loss of function 3rd degree sprain -Varus stress *no pain with unusable knee/increased mobility* -ligament ruptured

1. describe the etiology, the clinical appearance, and discuss the medical and physical therapy treatment for: a. *Osgood Schlatter's disease* -Etiology

*Etiology* 1. Osgood Schlatter's disease is *Osteochondrosis tibial tubercle*; Osteochondrosis = affects growth plate portion of bone 2. It is *self-limitng*, the pt. will go through the same 4 stages: Necrosis - Revascularization- Bone Healing - Residual Deformity; 3. You can also end up with an *Avulsion fx* if they continue with stressful activity; if mm get stronger than the bone the quadriceps tendon pulls on the tibial tuberosity -Activities like running, jumping, sprinting create a large amount of stress on the epiphyseal GP which is weak; body responds by laying down more bone that causes a deformity.

d. tears of collateral ligaments i. MCL -Etiology & Signs and Symptoms

*Etiology* 1. Valgus stress - Direct blow to lateral knee 2. Valgus stress + rotational stress -lower leg planted and twist away and upper body and upper leg rotated away form planted lower leg *Often in conjunction with *ACL and PCL injuries* *Signs and Symptoms* 1st degree sprain -Valgus stress *painful with NO increase in mobility* -minimal swelling or loss of function etc. 2nd degree sprain -Valgus stress *painful with moderate increase in mobility* -more swelling & loss of function 3rd degree sprain -Valgus stress *no pain with unusable knee/increased mobility* -ligament ruptured

1. describe the etiology and clinical appearance of, and discuss the medical and physical therapy treatment for: a. ACL injuries -Etiology = Contact vs. Non-contact

*Etiology* Contact: *1. Valgus-ABD type of injury* (most common) -Injury to medial aspect of knee; *2. Hyperextension* -Anterior blow to *distal femur* (2nd most common); -In CC it stops the posterior translation of femur on tibia Important to differentiate: -Anterior blow to DISTAL FEMUR= ACL -Anterior blow to PROXIMAL TIBIA = PCL because rustics poster tibia on femur Non-contact: Slightly flexed knee with valgus load with IR tibia or ER of femur - With the ER- you see the MCL injured first then the , Posteromedial cap, ACL, medial meniscus *Unhappy Triad = MCL, ACL, & Medial Meniscus* 1. Demographic 2. MOI Concomitant injury-Unhappy Triad: Usually won't be able to ambulate at all

f. compartment syndromes: -General MOI -Best step 2 types

*MOI* 1) Result with increased pressure within a closed location/compartment putting stress on neurovascular structures and mm; -Fascia that separates the compartments is thick and does not have much elasticity - if you have a lot of swelling in one of these you may worry about pressure building up in this compartment etc. be aware of what is in what compartment 2) *Best Step = NV* -check for pulses/sensations for appropriate nerves/arteries in that compartment; -if you feel decreased sensation/pulses and pt. is not getting better with rest - acute- send to ER 3) Two types we will discuss are acute and chronic

Tendo Achilles rupture -Treatment

*Non surgical* = immobilized with *long leg cast* -hope is that tendon will scar down *Surgically* = they can suture the 2 ends of tendon together -research says that there is no difference in management in non-surgical or surgical - but if athlete may want surgery but generally both ways the pt. recover fine

Plantar Fascitis - Treatment PT vs MD

*PT* -1) Find out cause of excessive stress on PF and treat that -2) Sometimes night splints can hold it in more stretched DF position - its more stretched/mobile = less stiffness; but not best for ppl with excessive pronation/DF because they are already stretching it! usually only for people with limited DF -3) Check for kinetic chain issues *MD* = may inject with cortisone; may do fascia excision and cut where it attaches to calcaneous (may create other problems)

PT Interventions

*Palliative:* -PRICE & Grades I and II to get rid of effusion *Preparatory:* -Soft tissue work/massage to improve blood circulation & help with swelling -Estim to quads *Corrective:* -Initiate motor control exercises- SLR and quad sets -Gentle PROM in pain fee -CC exercises progressed as tolerated -Strengthen hamstrings

Physical Exam & Treatment for Ankle Sprains -Findings -Best steps? -Treatment

*Physical Exam* AROM/PROM - decreased in beginning due to pain PROM C - same as AROM PROM A - hypermobility with lig laxity end feel ATFL - may have effusion; if its CFL no effusion; if PTFL (rare to happen alone) PTFL - intracapsular so effusion Best steps: 1. PROM A - best step 2. ST positive - ATFL anterior drawer test 3. PFT findings - why better than PROM C? because PROM C you are stressing multiple tissues - you don't know if pain if form ligament;s so for ankle - PFT is better step because you don't have a lot of mm; you can be sure you're in the right area May be inconclusive due to swelling - may have to re-do in Tx: 1. Beginning - PRICE with stability (esp. grade 2 or 3) 2. Dynamic Stabilization exercises/Proprioceptive exercises Ex: gastroc stretches, theraband exercises, heel toe walking, trampoline plyometrics later on -Also concerned with laxity (as swelling has gone down and ROM is restored etc, they think they can do more ) and recurrent injuries -Prone to having CAI (chronic ankle instability) - if pt. not following precautions or getting support/bracing or not dynamic stabilizing ex i.e. proprioception exercises; main predictor of having ankle sprain is having hx of ankle sprain - dynamic stabilization and proprioception important 2 things to keep in mind: 1. don't want them to have CAI 2. Need to provide them bracing or external support early on

Pros (3) & Cons of US (2)

*Pros:* 1) Low cost & portability 2) No known hazards - not putting anyone in small spaces etc. 3) Dynamic/real time *Cons:* 1) Steep learning curve - may take more training to use 2) Bone blocks some tissues for visualization

a) hallux rigidus = loss of motion at toe -Signs & Symptoms, Etiology, Intervention

*Signs & Symptoms:* 1. Decreased DF of 1st MTP 2. Pain and swelling in posterior dorsal aspect of joint 3. Pain and stiffness in MTP 4. Hx = difficulty walking (esp. uphill, climbing etc. anything required TO) 5. PFT = present on dorsal and lateral joint surfaces 6. AROM, PROMC and PROM A = positive findings *Etiology* = Adult population due to degenerative OA, Gout RA, Post trauma, intra-articular fx, excessive DF at MTP irritating it and getting arthritis leading to HR *Interventions:* 1. PRCIE principles if swelling inflammation; 2. Shoes with extra depth toe box or stiff sole to limit excessive DF; 3. Shoes with rocker bottom sole to limit excessive DF (motion that would generate pain) - but you still need at least 65 deg so if you limit it you may get other problems Lec: as PT can we correct it? Surgeons - replacement of 1st MTP joint, NSAIDs, steroids

Dual Energy X-ray Absorptiometry

*Uses:* 1) Measure total body composition/fat 2) Measure bone mineral density Has a LOW RADIATION! - Uses 1/10th intensity that normal X-ray would use

Why 2 Capsular Patterns?

-Hip joint is so deep -So many mm around it -Difficult to isolate the hip joint capsule -Variety: Hard to predict the exact pattern Lec: They had different methods; ones more NWB & ones more WB? -Cyriax is more NWB, Kaltenborn more WB

MRI T1 vs. T2

-MRI can do different waitings? T1 = more longitudinal *fat is very bright* CSF and other disc fluid is dark T2 = more transverse, fat is gray and CSF and discs are fairly bright

MRI vs. CT

-MRI is like CT, grayscale slices of tissues but NO IONIZING RADIATION - not based on X-rays! -*Superior method for viewing soft tissue detail and certain pathologies of bone i.e. brain tumors ets. -bone outer outline is really bright in CT, darker in MRI!

PCL Primary Roles

-Primary jobs: 1. Prevent posterior translation of tibia - OC Flexion 2. Prevents IR of tibia on femur

f. explain post-op precautions as would be instructed to a patient.

-no IR, ADD, or Flex above 90

ANKLE & FOOT 2 AND 3

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DIAGNOSTIC & ADVANCED IMAGING - did not look at!

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DEXA Results -T-score -Z-score -FRAX score

1) *T-score:* shows comparison of BMD with young women (30 years peak bone density years) -1 to +1 = Normal -1 to -2.5 = Osteopenia (thin bone) less than -2.5 = Osteoporosis 2) *Z-score:* shows comparison of BMD with other women same age 3) *FRAX score* = looking at what your fracture risk may be in about 10-15 years based on score now STOR - Simple calculated osteo something? (she talked about in class, not on ppt)

Diagnostic US

1) Images generated by reflected ultrasound 2) Reflective characteristics of tissue surface/interface: -Hyperehoic - reflect it back quickly i.e. bone because its dense - shows up dark -Hypoechoic - don't reflect back quickly - tissues don't show up as dark -Described with reference to surrounding tissues

iii. anterior tibiofibular ligament sprain - "high ankle sprain"

1. "high ankle sprains" = injury to the distal anterior and posterior tibiofibular Ligaments = ligaments that hold tibia & fibula together - its a syndesmosis! 2. Injuries are worse; why? - they take longer time to heal - problematic for people; once they walk they are WB and pushing talus up into ankle mortise and keep separating the tibia/fibula 3. MOI = forced ER and Eversion - landing on foot that drives talus up into tibia/fibula; usually some sort of twisting/rotation creating a shearing force that tears apart these ligs;

d. describe the four phases of osteochondrosis for: d1. pathogenesis. d2. radiographic appearance. Phase 1: Early Phase of Necrosis -Pathogenesis

1. Blood vessel damage 2. Bone deposition ceases in epiphyses, osteoblastic activity stops = osteocyte loss (basically the epiphysis starts to loose its mass) -No clinical signs, they don't feel anything they are asymptomatic - no one catches this phase -Usually the longest phase (3-5 months, whole process could take 18-24months), which is kind of unfortunate because symptoms aren't severe enough for you to do anything

Phase 3: Bone Healing

1. Bone resorption stops and deposition continues - its still laying down moldable bone but the process is lower than before 2. Granulation fibrous tissue replaced by bone - still not as good as normal bone and is still plastic and moldable

d. *Popliteus Tendonitis/osis vs. Semimembranosous* -Similarities

1. Both are *Flexor Mechanism disorders* -Medial Popliteal Area = ST and SM; Lateral Popliteal Area = BF and Pop; Medial and lateral gastroc also -Most injuries involve SM & Popliteus tendonopathy 2. Both Flex and IR the Knee 3. Both prevent excessive ER of tibia 4. Both have intracapsular attachments, so both could have EFFUSION -Pop to lateral menisucs & posterior joint cap -SM to medial meniscus & posteromedial joit cap 5. Both can occur as a result of repetitive trauma or overloading (like regular tendonopathies)

c. explain the etiology and possible predisposing factors leading to osteochondrosis.

1. Etiology is *idiopathic*: genetic? trauma? effusion? -trauma is just a theory 2. Its an adolescent disorder that affects growing children *3-10* -Prognosis is worse if on older end; deficits are less if it occurs at younger spectrum 3.*Males* are more likely (3-5x) than females -more active than females; more risky behavior 4. More likely in *LE* - Femur is most common place

d. identify the complications of prosthetic hip replacement that might necessitate a revision.

1. Femoral Stem Loosening -deep aching pain in thigh/hip; annoying because they can feel it moving around Pt. worse with weight, not getting better over time refer them back to get radiograph 2. Femoral Fx -deep severe pain in thigh that hurts with weight bearing 3. DVT/PE -blood clot in calf from immobilization after surgery; PE clot traveling to lungs -Present with swollen calf; catch DVT early before PE which could kill them -dizziness, fainting and SOB 4. Infection -look at incision site - any smells, pus, any nasty discharge i.e. green or yellow - infection and need to go back to surgeon After all surgeries you're going to have the dull achy pain etc. BUT if it does not get better after weeks and moths and gets more severe, worse weight bearing - refer them back Lec: why would females have more complications? -acetabulum is smaller, harder to control for the popping out etc.

Phase 4: Residual Deformity

1. Healing complete - bone is quality of bone; but Deformities may be present 2. Deformity present - may have leg height discrepancies; how would they stand? may IR and ADD hip (i think on taller side) 3. Cartilage initially normal 4. They can still have Degeneration over time Lec: Note that pics in this phase the femur is more rounded and in phase 2 its more flat limited hip motions all around but really rotation and flexion; end-feel is usually bony; mm around the joint not as developed as they should be i.e. atrophied glutes-- now becoming a biomechanics problem -Cartilage may be broken down; can't really do anything to stop it it just needs to take its course Management: -it will take its own course we just want to limit symptoms Brace in ABD to keep hip in neutral as it degenerates and hope that it won't shape as bad; Sometimes they break the bone to realign and put screws in i.e. these pt come in when they are 30 with degeneration and pain with no hx trauma -strengthen weak mm; stretch tight mm; improve joint mobility

Meniscal Tears -Signs & Symptoms

1. History: Clicking/locking/popping, giving way/buckling/instability -locking at all times = bad; its loose ends getting between the bones preventing motions at all times 2. AROM- pain with any - flex or ext because joint surfaces come together; Squatting can be painful or impossible 3. PROM- Gradually Joint effusion 4. PROM A - joint effusion with swelling EF; Hypomobility and Displaced meniscus end-feel (not sure if for PROM A or PROM c?) 5. MSTT - should be neg 6. Special tests: Macmurry (best- highly specific), something compression test *7. PFT-Acute joint line tenderness-(85% sensitive, 30% specific); very sensitive step* Lec: it will be hard to max stress in PROM A because we put them in LPP but MOI was with surfaces being compressed then torn; best step for TR? ST - Macmurry- is the best; its passive and maximal; next maybe PROM C is better than PROM A; still may find positive findings for PROM A though; PFT won't be for TR, but its good for TSI, also Hx; I think overall PFT and ST are good tests but ST may stress it more?

h. plantar fasciitis -Itis vs. Osis -Important Roles -Windlass mechanism

1. Itis vs. Osis -Inflammation = plantar facsitis -No inflamamtion = plantar fasciosis 2. Important roles: -1) Plays important role in supporting body weight - goes across longitudinal arch -2)Windlass mechanism: -@ HS/first part of stance phase it relaxes flattens arch and allows foot to accommodate to irregularities - also important for shock absorption -@ TO it tightens and causes the met heads to depress and longitudinal arch rises = it makes you foot ridged platform for propulsion -no function during swing phase 3. Acute - excessive loading of foot 4. Chronic - excessive midfoot or hindfoot pronation causing microtears in fascia; high arches - stress on fascia

Why is Medial Meniscus more prone to tears? 2 reasons

1. Less mobilityMM = can't get out of the way during movement = higher risk of 2. We always load medial compartment more during gait/running

iv. posterior talofibular ligament sprain

1. MOI: Severe ABD force or excessive Inversion; 2. Least common on the lateral side -very strong so doesn't get injured as much (one of the strongest); -also you would have to have excessive inversion 3. With this type of sprain you may have *dislocation, distal lateral mallelous avulsion or other tibiofibular fx* 4. Peroneal mm also involved Deltoid ligs - medial slide - also very strong - rare to injure compared to lateral side MOI: Excessive Eversion -stronger -less eversion

1. explain the functional significance of big toe MTP mobility.

1. Normally Need: 65 Degrees extension to Walk & 85 to Run 2. Important for Windlass mechanism - when they are extended during gait = pulls on plantar fascia = helps make rear foot more supinated/ridged/closed pack = needed for TO -Lack of extension = faulty windlass mechanism = more stress on plantar fascia during gait Cause of Limitations 1. Mm Tightness i.e. FHL 2. Joint pathologies i.e. Tight joint cap of 1st MTP or adhesions or effusions 3. Laxity could present as limited mobility -Could be mis alignment (biomechanically) = incongruence = limited motion Note: "Dorsal glide = anterior glide" & "Plantar glide = posterior glide"

ii. calcaneofibular ligament sprain

1. Often injured with ATF; more common than PTF 2. MOI: *Inversion but more in neutral* Findings: -Extracapsular - no effusion for PROM A -Damage to peroneal tendons may be apparent with this due to severe inversion

g. medial tibial stress syndrome -General -Exam -Treatment

1. Tibial periosteitis at attachment of Posterior tib or medial soles 2. Overuse Injury - Excessive stress/shearing force at interference of bone/tendon that could lead to swelling leading to MTSS "shin splints 3. Important to DD from stress fx, Posterior tibialis and anterior tibialis tendonitis 4. With MTSS = *More focal/local pain than compartment syndromes* *Exam* 1. Symptoms are in the anterior or posteromedial aspect of lower leg 2. Aggravated by exercises using LE 3. AROM - painful with PF and EV 4. PROM C - usually pain free; 5. MSTT - pain with resistant PF and EV 6. PFT - tenderness in posteromedial calf *Tx - Adress impairments you find* -Fist work on decrease swelling and pt. education/activity modification to stop activity to bring swelling down; -tx any mm weakness, tightness, joint mobs probs

Treatment - Operative

2 types of surgery: 1. Menisectomy: shave or excision of meniscus 2. Repair Why do we need to know which one? -Repair? = there are sutures to hold together; early WB not allowed; we need to protect tissue -Shaved? = 1-2 days you can WB; sometimes they may need to slow down because they dont feel those symptoms anymore - could aggravate it more; you still need some protection for it to heal Lec: when would someone be a candidate for surgery? Look at function, their goals, pain etc. also time - why time? if you don't see any improvement in any interventions aka not responding to your treatment you eighteen reevaluate them or go get an MRI; also tissue - something like muscle can eventually have deposits and cartilage acts different (wasn't sure)? Also depends on if tear is at periphery or central

b. PCL injuries -Etiology: How could you injure your PCL?

Any force that drives tibia back on femur 1. Falling on flexed knee 2. Direct blow to the anterior aspect of tibia. 3. Forced hyperflexion - (MVA) "dashboard" injury 4. Fall onto tibia - where the tibia is forced posteriorly -Really any blow below the knee or to the proximal tibia pushing it back = PCL Usually pt. can function without surgery *Rare and Mostly in conjuction with ACL/MCL/LCL

TKA Radiograph

Artifictial metal more radio-dense = appears white on radiograph

Phase 2: Revascularization -Radiograph

As child grows and puts stresses on it the head gets flatter- you may see a flatter femoral head and possibly fractures

b) hallux valgus = position of toe Prevalence & Intervention

As you pull great toe into ABD position to correct it - coincides with a medial glide Prevalence: more common in women than men 9:1, mostly older women and people who wear high heels Interventions = same as HR!

General LCL

Attachments: Lateral Epicondyle to femoral head. -No att. to meniscus so joint effusion is not common- should not have any PROM A positive findings Taut in full Extension, ADD & ER of tibia on femur Restraints excessive Varus force VPP: injured less because we don't load lateral compartment as much

Metatarsalgia VS. Morton's neuroma

Best 2 steps to differentiate *Metatarsalgia* 1. PFT - Tendernes underneath met heads 2. NV/Sensation testing - no nerve/sensation involvement *Morton's neuroma* 1. PFT - Tenderness in-between met heads 2. NV/Sensation testing- nerve/sensation involvement, you'd feel tingling and numbness Both = Chronic compression due to faulty shoes or injury to ligaments resulting in excessive stress; increased symptoms with weight bearing that is relieved with removing shoes or massage

c. coxa vara. d. coxa valga. e. coxa plana.

Coxa Vara & Valga = in Frontal Plane Anteversion & Retroversion = in Transverse Plane

c. Posterior fracture-dislocation of the hip

Etiology: -Dashboard injury: LE in Flex, ADD and IR - how leg is riding in car Medical Emergency: -BV damage = decreased BS to femoral head -Sciatic nerve = foot drop Radiograph: Dislocation of femoral head posteriorly & Fx of Acetabulum Treatment: ORIF of Closed Reduction Outcomes: AVN, Sciatic N, Post-Traumatic DJD

Degenerative Joint Disease

Etiology: -Primary and secondary -Biomechanical factors: Exam: -Gradual onset, weight bearing/compression pain Treatment: -Conservative (PT) or Surgical (usually THR) Lec: Lec: what kinds of biomechanics? 1) Marked mm. asymmetry and weaknesses forcing joints in certain positions - abnormal forces on jt; 2) Mal-alignment - varum -weight plays a big part- if you're heavy it could affect the amount of weight you put thru your joint -Age also plays a factor

c. *Pes Anserinus Tendonitis/osis - SarGT* -Etiology

Etiology: 1. Tight HS mm 2. Direct blow to the medial aspect of knee 3. Repetitive use = i.e. soccer, dancing; placing stress on medial knee 4. Look at Foot! - Exceessive Rear-foot pronation causes excessive stress on medial aspect of knee - Valgus stress 5. Look at Hip! - Weak glutes increased medial/valgus stress

c) hammer toes vs. claw toes

Etiology: 1. Usually due to mm. imbalances - weak intrinsics and stronger extrinsic - pulling toes in to abnormal positioning of toes; 2. Capsular contractions at IP joints 3. Also could be due to structural changes *Hammer Toe* Extension of MTP and DIP Flexion of PIP* -Usually only effects 1 toe (2nd) *Claw Toe* Hyperextension of MTP Flexion PIP and DIP -Pes cavus and neurological disorders

b. femoroacetabular impingement = FAI = Hip impingement -2 types

Etiology: Impingement can happen with excessive flexion where the femur and acetabulum get impinged 1. Cam Lesion: abnormal *femur* head/neck junction -the femur is kind of over protruding 2. Pincer Lesion: *acetabular* overcoverage -more of the acetabulum 3. Can be MIXED ^^ these are the structural problems that could lead to impingement Exam: 1. Pain - anterior hip/groin 2. PROM C: Flex & IR (tend to go in these directions) 3. FABER, Scouring - ST Interventions: -Conservative (PT) and Surgical Lec: PT: they may have muscle imbalances; may need to look at the capsule mobility for any defects (if they go into flex/IR then the anterior portion must be tight) then strengthen

PCL Injuries -Physical Exam

Exam findings will depend on the grade of the sprain! *Pain:* none to minimal (but present during ST) (G1), yes (G2), maybe at beginning but eventually no pain (G3) *Laxity:* none (G1), moderate (G2), significant (G3) *Swelling:* Minimal swelling (G1), swelling (G2), diffuse swelling (G3) *Motion:* Normal to decreased (G1), decreased (G2), possibly increased (G3) *Loss of function:* minor (G1), moderate (G2), complete (G3) *(+) Special tests:* Post. Drawer, post. sag, Godfreys, reverse Lachman *PROM A:* unremarkable! -PCL fibers do not blend with capsule so no Effusion/PROM A findings

2. name three common symptoms and signs of patello-femoral pain syndrome .

Examination - PFPS is not a TSI 1. Anterior knee pain 2. Pain with prolonged sitting, squatting, stairs - aka knee is in flexion - commonality = causing PFJ compression -may hear a "pop" when they stand up - "movie-goers or students" knee = prolonged sitting 3. Gradual onset most of the time

IT Band Friction Syndrome -Physical Exam & Management

History? PFC AROM PROM MSTT: positive for mm action - if tendon is the reason MLT: positive for lengthening - i.e. if TFL is tight MMT ST: Nobel's compression-Patla's variation PFT-Over insertion Gerdy's tubercle/lat. Or ant.knee (TR step - need to find the tissue first! Its a syndrome so you need to be more specific ) Pain radiates towards prox tibia increases with activity mostly with flex; localized lateral knee pain over condyle (2 cm above joint line) or diffuse deep anterior knee pain; symptoms/Pain during the activity - jumping equating, kneeling,

Computed Tomography (CT scanning)

Involves a radiograph -produces images based on the same principles -X-rays are passed through the tissues in a 360 arc -recorded by a series of electronic detectors -multiple slices, axial and 3-D

2. describe the signs and symptoms and clinical findings of *Iliotibial Band Friction Syndrome.*

Is it a TSI? No even though its specific you don't really know where the friction is or the reason for it; the TSI will be what the reason for the friction is Possible TSI: 1. Tight TFL 2. Excessive femoral anteversion or retroverison Function: 1. Pulled Anterior in flexion via TFL 2. Pulled Posterior in extension via G max -Crosses the lateral epicondyle - goes back in forth during knee flex/ext = can cause friction 3. Its a knee extensor from 0-30; above 30 its a knee flexor *Any clicking, popping, pain = IT Band Friction

d. *Popliteus Tendonitis/osis vs. Semimembranosous* -Physical exam

PFC: inflammation or not for itis vs. osis AROM: positive for mm actions PROM C: positive for opposite mm action; but for SM because its 2 joint you may not have positive findings; but you could have positive findings for pop PROM A: Could be positive for effusion MSTT: positive for action MLT: positive opposite of action MMT: Deferred PFT: positive depending on depth and location TR: MLT 1st then PROM C (abnormal mm end feel)

General Treatment for ACL injuries -Conservatively/PT -Non-Conservatively/Surgery

PT/Conservative: -Think with any ligament issues you should brace it for support initially! 1. Treat Effusion 1st! 2. No Terminal Knee Extension exercises 3. No excessive Tibial Anterior Translation! - Occurs during OC extension via quads so you would not want to strengthen those -Tx ROM should be between 90 flexion & 45 extension to avoid anterior trans 4. Start in CC for Co-contraction of Quads & HS; don't start in OC 5. Strengthen Hamstrings to control the amount of anterior translation 6. Progress the CC exercises as tolerated 7. Gentle PROM as tolerated by pt. Surgical: -Usually surgeons want PT before surgery and usually try to send the pt. to PT before doing anything -Use an autograft or an allograft; Auto graft comes from yourself (patellar or HS); allograft comes from somewhere else

a. trochanteric bursitis -PT vs. MD Treatment

PT: Decrease friction & inflammation -never use "US by itself" on test (i.e. put in thermal/non-thermal) -activity modi faction - important -ST mobilization ("milk the burase") -Exercises? AROM in PFR! Getting it activated w/o irritating it MD:

3. define chondromalacia patella.

Pathophysiology Softening/ or wearing away of articular cartilage on undersurface of patella Physical Exam Radiograph or arthroscopy No clinical tests to confirm -Hx they will say pain with the typical squatting, sitting etc. may say they have clicking, popping, crepitus but still need imaging to confirm -PROM A findings: cartilage is inside capsule so these can be positive; you would find hypo-mobility because they will stop using the joint; EF? Abnormal Cartilage - hear the crepitus/roughness etc.; you could also get tight capsule, swelling, maybe adhesion So TSI will probably be Joint Capsule - PROM A is best step for reactivity VPP: we can't make this diagnosis as PT, imaging is required; you will learn more in MSK with patellar manipulations and palpations -Layman's term its OA of the joint

4. compare and contrast the etiology, clinical examination, and physical therapy management for hip tendinopathy including: a. iliopsoas tendinopathy

Same general concepts used for UE tendinopathy applies to these

TKA Prevalence

Performed since 1970's More than 581,000 TKA per year in U.S. AAOS expects number to double by 2030 Average patient age= 70 Female greater than male, 1/3 considered obese *Problem?* We don't get them early enough! As PT we can meet with them pre-op etc. PT can prevent these surgeries but sometimes pt. aren't educated enough that they can opt for PT; And we need to be successful in preventing things So educate them about non impactful activities like cycling rather than running - need to be aware that if they continue with intense activities they may have more issues and could lead to early revision

Plica Exam

Physical Exam - 1. PROM acc - in joint cap so you can have findings 2. Plica Stutter Management- swelling, ms. imbalance, Massage-CFM, relieve stress/load, MT techniques. Surgery- Arthroscopic excision Lec: How do you make hypothesis? look at hx - may have changed something i.e. running more/changing workout resulting in aggravating tissue Tx will be similar to treating bursa - PRICE, activity mod, soft tissue work - waiting to calm down; then later find if any mm imbalances or tight joint cap - find out why it was inflamed in the first place -You can do patellar glides

What are some potential *complications* of a tibial plateau fracture?

Potential Complications 1. Intra-articular adhesions 2. popliteal nerve damage (initial injury or cast too tight) 3. DJD -Peices may not come together in same way they originally were = wear and tear on those joints 4. Stiffness due to immobilization If they had external fixation need to pt. education on infection!

d. *Popliteus Tendonitis/osis vs. Semimembranosous* -Management

Same treatment for tendonopathies Tendonopathies are usually result of a problem not the cause! TREAT THE BIOMECHANICS Itis - Reduce swelling, inflammation etc. Osis - Reactive or Degeneartive? Reactive: Reduce load & activiy mod Degenerative: Load tendon heavily and work toward eccentric

PCL Treatment -Which groups would you want to rehab?

Similar to ACL but different muscle groups! 1. Don't need to treat effusion for PCL, but PRICE principles still initially 2. Terminal Knee Extensions are good here! 3. Avoid any posterior translation of tibia 4. Strengthen Quads in beginning to limit the amount of posterior translation! - Don't want to strengthen HS 5. PROM should be in full range to passive knee extension 6. Patellar mobility important 7. Grades 1 and 2 usually WBAT; Grades 3 - surgery 8. Long leg braces for grades 3 due to ligamentous laxity

5. describe the influence of kinetic chain abnormalities on abnormal stresses to the patello- femoral joint, in terms of the: a. calcaneus, talus, tibia and fibula, and femur position, statically and dynamically b. muscle imbalances.

look at hip, knee and ankle positioning during functioning activity; In pic: theres genu valgum hip lower on one side compared to other - trendelengburg gait = weak ABD Q- angle: lateral patellar tracking in cc is happening; again its usually the weakness in hip thats causing it

Total Knee Arthroplasty

slide 26 = Femur could crack during surgery; see pt. = try to put on crutches/walker - want WB for wolfs law - healing; want them to get up and move; make sure to look at OP reports - i.e. 20% WB because femur fractured; if you didnt read it you could do more WB and end up hurting them Basically anytime you get these pt. up and moving make sure you've talked with the surgeon or looked at op reports to see for any special restrictions depending on how surgery went; Also joint mobilizations - you may not be able to mobilize new components - not all prostheses are the same - some may not allow this; you wouldn't know this unless you looked at OP report or talked to surgeon Reasons why TKA; pain in knee interfere with function - to relieve pain and improve function; or advanced DJD, infection, RA, avascular necrosis etc. Lec: Main thing to keep in mind with surgery = Operative Note- this will make you evaluation results different and you need to be aware of it; Protocols are important but they are very general so they can be tweaked