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					CM Exam 3
Non-Traumatic Knee Injury
     History: IMPORTANT
          o MOI, Snap? Able to bear weight? Could you continue with activity? Ever happened before?
             Anything help? Other sx? Swelling?
     Exam
          o Inspection: skin, effusion, position, gait analysis
          o ROM
          o Palpation: boney, soft tissue, pulses, effusion, sensation
          o Strength Testing: 5/5 is best
          o Ligament Testing (Special testing) – feel “endpoint” with normal ligament fxn
                  MCL Valgus at 0 (capsular integrity) and 25 (ligament itself) degrees
                  LCL Varus 0/25
                  ACL: Lachman’s, Anterior Drawer
                  PCL: Posterior Drawer
          o Meniscal testing (Special testing)
                  McMurray’s
                  Bounce Home
                  Apley’s Grind
          o Functional Techniques
                  Think “kinetic chain” (how are quads?)
                  Understand pronation (most weight on medial foot) and supination (most weight on
                     5th metatarsal)
                  Understand “Real world” muscle function
                  Understand influence of compensatory and accommodative mechanisms
     Imaging: may not be needed; dx based on hx and clinical eval
          o Typical: plain films, bone scan, US, CT, MRI
          o XRAY: Assess arthritis, growth plate injury, loose body, joint effusion
                  Get AP VIEW STANDING – to see true alignment and joint space narrowing
                  Usually 4 views: Bi-lat, standing AP, 30degree “Merchant” view for patellar tracking,
                     and “Tunnel” view
     Intrinsic Risk Factors for Overuse Injury
          o Biomechanical
                  Malalignment
                  Leg length discrepancy
                  Poor flexibility
                  Pronation vs. supination
                  Foot type
          o Age
                  Pediatric: rapid growth increases injury risk, Physis infrequently injured, Apophysis
                     frequently injured
                  Middle-age: Inadequate conditioning and flexibility, Poor insight and judgement,
                     “weekend warrior”
                  Senior athlete: Watch for underlying disease process, medication may alter
     Extrinsic Factors for Overuse
          o Mechanical: shoes, surfaces
         o Coaching
         o Environment/Equipment (stretching, strengthening)
         o Drug Use: ergogenic, therapeutic
         o Training
   Classification of Overuse Injuries
         o Grade I: Pain after activity only
         o Grade II: Pain with activity, does not restrict performance
         o Grade III: Pain with activity/significant performance restriction
         o Grade IV: Pain with activity and rest
   Case 1: A 28 yo female elite recreational runner presents to your office with “pain in the front of
    my knee”. She has recently moved to Blacsksburg from Kansas and notes that “running on these
    hills is killing me”. She points to the junction of the patella and the quadriceps muscle when
    describing her pain. There is no swelling, locking or giving way. No hx of knee surgery. She’s had
    occasional knee pain in the past dx’d as “runner’s knee”. She’s used ice and OTC meds prn. She can
    still run but has cut her distance down and notes that running down hill really flares up her
    symptoms. Her shoes are well worn (they are my favorites) and she has no idea how many miles
    they have on them but she’s had them for 1 ½ years and runs about 50 mi per week.
         o Exam: No swelling or effusion. Full ROM with mild discomfort with hyperflexion. No joint
             line tenderness. Ligamentous exam normal. Increased foot pronation and long leg on
             injured side. Tender at junction of quads and patella.
         o Diagnostic Testing: Not necessary
         o Dx: Anatomic long leg, compensatory functional pronation, Quadriceps tendonitis
         o Tx: Custom orthotics with heel lift. OMT. NEW SHOES. “Relative rest” (decrease mileage,
             cross-training; no hill running). Short course of NSAIDs – taken regularly.
   Pathomechanics of Tendonitis
         o Chronic tendonitis/tendonosis
         o Acute Tendonitis
         o Major Causative Factors
                   Two broad categories: Changes in mechanical loading, Changes in muscle tendon
         o Intrinsic Factors: Structureal failure secondary to overload, weakness, or a combo
         o Extrinsic: Impingement b bone or other structures
         o “Choking the Tendon”
   Case 2: A 13 yo male BB player presents to your office with a painful “lump” on the front of his
    knee that’s been getting progressively larger over the last few months. There is no history of
    trauma. Mom says he plays sports “all the time”. He’s grown about 4 inches over the summer. She’s
    worried that he must have a “tumor or something”. Sometimes the bump gets a little red. The
    athlete notes that it’s really starting to affect “my game”. Hurts a lot to jump.
         o Exam: No swelling or effusion. Redness over “bump” on proximal ant tibia. Very tender
             here. Full ROM. Ligamentous WML. Tight quad on affected side
         o PLAIN FILMS
       o Tx: “relative rest,” Enhance strength and flexibility (PT). Ice and OTC analgesics. Brace.
   Pediatric and Growth Issues
       o Apophyseal Injury: results from traction induced microtrauma at tendon-bone junction
       o Physeal injury: result from repetitive loading. This may cause metaphyseal ischemia and
           poor growth in proliferative zone that results in widening or narrowing of growth plate.
   Osgood Schlatter’s Disease
       o Background: Common cause of knee pain in active adolescents. Dx is usually made on basis
           of characteristic localized pain at tibial tuberosity; radiographs not needed for dx.
           However, radiographic results confirm the clinical suspicion of the disease and exclude
           other causes of knee pain.
       o Pathophys: Originally thought to be from avulsion of bone or cartilage in tib tub. But more
           recent findings indicate most cases are caused by microtrauma in deep fibers of patellar
           tendon at its insertion on tibial tuberosity.
       o More boys than girls. 10-14 years.
       o Usually self-limited. Sx resolve with skeletal maturity when tib tub fuses to tibia.
       o Lateral XRAY of knee. AP for r/o other conditions. No CT or MRI
   Popliteal (Baker’s Cyst)
       o Distended bursa within popliteal space. Most common bursa to become involved lie
           beneath the medial head of gastrocnemius muscle or semi-membranous tendon.
       o Patients present with complaint of aching pain in post knee or prox calf.
       o XRAY first.
       o In adults, Baker’s cysts are most commonly associated with intra-articular pathology.
       o Tx: popliteal cysts are primary condition and rarely assoc with intra-articular path.
           Pediatric cysts may be bilateral and usually resolve with time. Occasionally excision is
                In adults, if intra-articular path has been treated and discomfort still remains,
                  surgical excision. Can be aspirated, but recurrence is common.
   Sinding-Larsen-Johansson Syndrome
       o Inflammation of patella at its inferior pole. Origin of patellar tendon; traction injury
       o SS:
                Slightly swollen, warm, and tender bump below the kneecap
                Pain with activity, especially when straightening the leg against force (such as with
                  stair climbing, jumping, deep knee bends, or weightlifting) or following an extended
                  period of vigorous exercise in an adolescent
                In more severe cases, pain during less vigorous activity
       o Tx:
                  Ice to relieve pain, stretching and strengthening exercises, and modification of
                 kneeling, jumping, squatting, stair climbing, and running on the affected knee
                   should be avoided
                 A patellar band (brace between the kneecap and tibial tubercle on top of the patellar
                   tendon) may help relieve symptoms
   Case 3: A 45 yo female recreational runner and multisport athlete presents to your office with a
    many year hx of intermittent ant knee pain which responds transiently to rest, ice and anti-
    inflammatory meds. She reports being “fed up” with the problem and wants to get to the bottom of
    it. She notes pain with stair climbing. If she sits in a movie and then tries to walk she has
    significant pain which gradually resolves over several minutes. She has had no swelling or locking
    but occasionally feels that the knee “gives out”.
         o Exam: Gait eval in the hall shows valgus influence at the knees and bilateral increased
            pronation at the feet. She has tight hamstrings bilat and poor VMO tone. She has increased
            patellar mobility bilat and a mildly + “apprehension” sign. Mild peri-patellar tenderness. No
            effusion or instability on ligamentous exam
         o Get plain films
         o Dx: (can use for SP DDx)
                 Patellofemoral Pain Syndrome
                 Bilateral hyperpronation
                 Lower extremity inflexibility and VMO insufficiency
   Patellofemoral Pain Syndrome
         o Multifactorial etiology
         o Causes include overuse/overload, biomech problems and muscular disfxn
                 Pes Planus (Pronation)
                 Pes Cavus (High-Arched Foot, Supination)
                 Q Angle
                 Muscular Causes

       o Patella Tracking
             Tilt
             Subluxation – increased lateral movement as knee is extended “inverted J”
             Apprehension test
                     Lateral pressure and pt feels like the knee is going to “pop out”
             Comprehensive functional biomechanical evaluation
         o Tx: Rest, quad strengthening, eval of footwear/orthotics. OMM. Icing, esp after activity.
            Knee sleeve.
     Osteochondritis Dissecans
         o Unknown etiology
         o Sx include general pain with swelling and/or aching, esp after activity
         o Intermittent knee pain and mild swelling that just “never gets better” – the knee sparin that
            keeps on hurting
         o Most commonly found on medial femoral condyle weight-bearing surface.
         o Dx by Xray (Tunnel View), shows radiolucent defect, typically on femoral condyle, confirm
            with MRI
         o Tx: Rest. Non-healing leasions may require period of non-weight bearing and/or surgery
         o 90% of knee non-traumatic problems and injuries can be accurately diagnosed with a good
            history, physical exam and plain x-rays
         o MRI is seldom needed but often requested by the patients
         o History alone will allow accurate diagnosis up to 70% of the time
         o Don’t interrupt the story and the patient will tell you most of what you need to know
     Summation
         o Always examine the uninjured knee first
         o Save the most painful test for last!
         o Order appropriate diagnostic studies
         o Refine diagnosis as appropriate
         o Address kinetic chain dysfunction and treat osteopathically

DDx of Knee Pain
     Knee Pain
         o Approx 1/3 musculoskeletal problems seen in primary care settings. Pain in up to 20% of
            adult population
         o Stress point: force on patellar tendon as high as 17.5 times body weight in weight lifters
     Knee Anatomy
         o Double condylar, complex synovial articulation
         o Cartilage
         o Ligaments
         o Move in three planes at once:
                 Flex and extend
                 Translate varus to valgus
                 Rotate (medial condyle is longer, resulting in posterolater (ER) of tibia with full
                   extension/Anteromedial (IR) glide with flexion)
   Knee Exam: Hx
       o Knees wear out and get injured in predictable patterns. (Most of us break the same way)
       o OLDCARTS
              Onset (acute or chronic)
              Location
              Duration
              Character
              Alleviating/ aggravating factors
              Radiation
              Timing/Treatment
              Severity
       o Age
       o Occupation
       o Functional loss
       o Past Medical/Family History
       o Mechanical symptoms (locking, popping, giving way)
       o Joint effusion (timing, amt, recurrence)
       o Specific MOI
              Anterior blow to tibia (i.e. dashboard knee)
              Lateral/medial blow to the knee
              Noncontact blow to knee
              Hyperextension
              Sudden twisting
       o Difficult to get right dx the first time – often pt is in too much pain to relax and get good
          exam. Exclude infection, fx, and neuro injury (bad stuff) and re-eval in a few days.
       o Review Predisposing factors
              Prior injury – including spine, pelvis, hip, femur, tibia, fibula, ankle, foot, as well as
                 the knee
              Structural abnormalities – scoliosis, pelvic obliquity, femoral torsion, leg length
                 discrepancy, tibial torsion, ankle or foot deformity
              Weak or imbalanced muscles
              Leg length discrepancy
              Pathologic inflexibility or hyperlaxity
              Any other Osteopathic Somatic Dysfunction
   Knee Exam: ROS
       o Joint pain (arthralgia)
              One joint suggests trauma, bursitis, tendonitis, osteoarthritis
              Polyarticular migrating pain suggests rheumatic fever or gonococcal arthritis
             Polyarticular, progressive, symmetric pain suggests rheumatoid arthritis
      o Stiffness/loss ROM
             Loss of AROM and PROM? Suggests articular pain
             Loss of AROM, but not PROM? Suggests non-articular pain
      o Muscle pain (myalgia) or weakness
      o Swelling or redness
             Trauma?
             Inflammatory? (ie gout)
             Infection? (ie septic arthritis)
      o Skin
             Consider SLE, psoriasis, gonococcal, Lyme
      o Neuro
             Paresthesias, weakness, radicular symptoms
      o HEENT
             Consider Reiter’s (can’t see, can’t pee, can’t climb a tree), Bechet’s (big mout ulcers)
      o GU
             Consider Reiter’s or gonococcal
      o GI
             Consider UC, enteritis
   Common Differential Dx

   Anterior Knee Pain
       o Patellar subluxation/dislocation
               5x higher in 10-17yo
               MOI: Valgus stress and IR of thigh (sports 61%, dance 9%)
               Sx include “giving out” or “giving away,” effusion
               Dx by hx, positive patellar apprehension sign
               Xray, MRI
               May be assoc with articular cartilage injury (surgical repair)
               Immobilization (3-6 wks, PT)
               With dislocation, high percentage of re-injury
       o Osgood Schlatter
               Ant. Tib pain
               Gradual onset; worse with squatting, jumping, stairs, quad contractions
               Tender to palpation over tib tub
               Tx: ice, modification of activity, NSAIDs, patellar strap, OMM
       o Patellar tendonitis aka Jumper’s Knee
               Typically teenage boy w/ recent growth spurt
               Gradual onset; worse with squatting, jumping, stairs, quad contractions
               Tender to palpation over patellar tendon
               Tx: ice, modification, NSAIDs, patellar strap, OMM
       o Patella Tendon Rupture
               MOI: fall with flexed knee…big pop and then can’t extend knee
               30-60yo
               SS: significant pain/swelling, instability, inability to extend knee
               Tx: Surgical repair
       o Sinding-Larsen-Johansson Disease
               Traction apophysitis
               Teenage growth spurt
               Gradual onset; worse with squat, jump, stairs, quad work
               Tender to palpation over distal patella
               Tx: ice, modification, Nsaid, patellar strap, OMM
      o Patellofemoral Pain Syndrome; aka Chondromalacia
              Typically vague hx of mild to moderate pain
              Worse with prolonged sitting (aka theatre sign)
              Overuse, overload, biomech, muscular disfxn
              Pain reproduced with direct pressure on patella, apprehension, inverted “J” sign
              Tx: Rehab, NSAIDs, knee sleeve, ice, OMM
   Medial Knee Pain
      o MCL: most common ligament injured in knee
              MOI: Valgus force and ER of tibia
              Sx: Medial knee pain, soft tissue swelling, instability
                      DDx includes meniscus
              Dx: hx, laxity/pain on valgus stressing, tenderness over ligament

                   I: tenderness, no laxity
                   II: inc laxity <5mm
                   III: inc laxity, >5mm, no end point (Think of other injuries as well!)
                   Tx I and II: NSAID, bracing
                   Tx III: mostly conservative; surgery with other injuries (avulsion fx,
                      continued instability)
       o Meniscus Tear (could also be lateral)
            MOI: rotation over planted foot or collision
            Medial >>> lateral
            Sx: “snap” or “pop” with injury, “clicking” or locking, “going out/giving way,
            Dx: hx, McMurray Test, Apley compression, joint line tenderness
            Surgery (arthroscopy): meniscectomy vs. repair
            ZONES: red has good blood supply, white doesn’t

       o Medial Plica Syndrome
            Redundancy of joint synovium
            Acute onset
                 Typically overuse
                 Tender thickened plica (medial retinaculum)
                 Tx: NSAID, ice, steroid injection, rehab, OMM

       o Pes Anserine Bursitis
               Insertion of Sartorius, Gracilis, Semitendinosis (Say Grace before Tea)
               Tender of anteromedial aspect of prox tibia
               Typically overuse or trauma
               Tx: NSAID, ice, steroid injection, rehab, OMM
   Lateral Knee Pain
       o LCL
               MOI: Varus force, hyperextension or ER (most common traffic accident – hit from
                  side =MCL one side, LCL other knee)
               Sx: lateral knee pain, soft tissue swelling, instability
               Dx: hx, laxity/pain on valgus stressing, tenderness over ligament
               Tx: Grade I/II: conservative; Grade III: surgery
       o IT Band syndrome
               Most common cause of lateral knee pain in runners, overuse, strength deficits in
                  abductors, leg length discrepancy
               Ober’s test, modified Thomas test
               Tx with NSAIDs, ice, steroid injection, rehab, modify activity, OMM, foam roller
       o Baker’s Cyst
               Originates from posteromedial knee joint
               Insidious onset of pain
               Palpable fullness of medial aspect of popliteal area; often associated with
                  meniscal tear
               Aspiration, but surgery better
   Knee Pain
       o OA: common in pt over 60yo
               Pain aggravated by WB activities, relieved by rest; morning stiffness
               Decreased ROM, crepitus, mild effusion
               Tx: NSAID, Tylenol, ice, exercise, bracing, OMM
       o Infection vs. Arthropathy
               More common in pts with cancer, DM, EtOH, HIV, Steroids
               Absence of trauma
               Knee warm, swollen, exquisitely tender, decreased ROM
               Diagnose with arthrocentesis
               Staph, Strep, H. influencza, N. gonorrhea
               Sodium urate crystals (Gout) vs. Calcium pyrophosphate (pseudogout)
       o Osteochondritis Dessicans
             Acquired lesion of subchondral bone with or without articular cartilage involvement
             Most common over medial femoral condyle
             Nonspecific knee pain, exacerbated by exercise, intermittent effusion
             Adults may have mechanical symptoms ( meniscal tear in DDx)
             Xray (tunnel) and MRI to eval
             Tx
                    Conservative: ½ kids will heal. Physis is open, 10-18 months, compliance
                       with rehab. Immobilize for 4-6 weeks; rehab 6-12 weeks; gradual return to
                       activity. Hard to do, so use surgery
                    Surgical: adults, unstable lesion, unresponsive to conservative
       o ACL: primary restraint to anterior tibial translation
             MOI: often non-contact
             Dx by hx: instability, acute effusion; positive Lachman’s, Anterior drawer; MRI to
             If non-operative course, Risks include: Meniscal injury, early onset OA, failure of
                secondary stabilizers
             Imaging: Segond fx
             Gender: ACL 9x in females; biomechanical and neuromuscular factors have been
                IDed as most compelling contributors (MSK stability of leg during dynamic impact-
                loading tasks)
       o PCL
             MOI: direct force against anterior tibia (MVC “Dasboard knee,” sporting
             Dx: Hx (instability, effusion; positive POSTERIOR DRAWER, Sag sign; MRI to
             Tx: Conservative (PT, NSAIDs). Surgery used occasionally in high-performance
                athletes (LOOOOONG REHAB)

   Knee Imaging: most are negative
       o Ottawa Rules (in Canada…good rules for Primary care in states)
              Age >55 or <18 years
              Isolated patella ttp
              Fibular head ttp
              Inability to flex knee to 900
              Inability to weight bear after injury or in ED for 4 steps
              ↓ knee radiographs by 25-50%
                     Sensitivity 97-100%
                     Specificity 27-49%
       o Can the decision rules apply to kids?
              Incomplete fused physes; injure epiphyseal plates more with trauma
              Inability of young children to localize pain
               Dependent on kid’s ability to ambulate independently
       o Pittsburgh Rules
               History of blunt trauma
               Fall as mechanism of injury
               Age >50 or <12 years
               Inability to weight bear for 4 steps
                      After injury or in ED
                      Heel pad to toe pad for each foot
   Knee Imaging
       o Acute injury: AP and lateral views
       o OA: bilateral AP standing and sunrise to allow for all 3 joint compartments (medial, lateral,
       o Mechanical symptoms/trauma: Tunnel view (45degree flexion) to look for loose bodies
       o PFS/Patella subluxation: “Merchant” view (30degree flexion) to better assess patellar tilt
          and groove. (merchant: compare both knees on same plate)
       o Subjective
               History of present illness (OLDCARTS)
               Review of systems
                      General
                      Musculoskeletal
                      Neurologic
                      Gastrointestinal
                      Genitourinary
                      HEENT
               Past Medical/Surgical /Family/Social History
               Medications
               Allergies (reaction)
       o Objective
               Vital signs
               Physical exam
                      General
                      Musculoskeletal
                      Neurologic
                      Osteopathic
                      Gastrointestinal
                      Genitourinary
                      HEENT
       o Assessment
               Most likely diagnosis
                      Osteoarthritis
               Differential diagnosis
                      Meniscal tear
                      Osteochondritis dessicans
                      Arthropathy
               Other diagnosis
                      Leg length discrepancy
                      Tobacco abuse
                      Hypertension
               Osteopathic diagnosis
                          Somatic dysfunction of pelvis
                          Somatic dysfunction of lower extremity
         o Plan
                   Medications
                   Labs
                   Imaging
                   Referrals
                   OMM
                   Prevention
                   Follow up

Lyme Disease
     Before-Lecture Statements
          o No proof that long-term antibiotics cure chronic lyme disease
          o Tx should work in 2-4 weeks
          o Most have positive Lyme titer…doesn’t mean you have disease (PA, MD, MN)
          o Highly assoc with arthritis (knee most common)
          o Secondary to systemic infection from spirochete
          o Deer Tick
          o Manifestations: acute infectious phase
     Most important symptoms in skin, heart, CNS, eyes
     Three Stages: early localized, early disseminated, chronic disseminated (curable with antibiotic
          o Localized infection will progress in approx. ½ of untreated pts
     B. burgdorferi: inflamm response in skin explains multiple lesions of erythema migrans
          o Abs will be present in most tissues (in CSF = CNS penetration)
     MOLECULAR MIMICRY produced by B. burg generates AI inflammatory reaction
          o Pathophys early vs. late = syphilis
          o B. burg induces immune response which may produce sx with little evidence of
             bacterial invasion of affected organ
     Lyme arthritis is associated with production of proinflamm cytokines and formation of immune
      complexes, and genetic factors (HLS-DR4/DR2)
          o Patients with HLA haplotype DR4 or DR2 and antibodies to OspA and OspB proteins in
             their joint fluid may be more susceptible to long-term arthritis.
     Lyme disease fastest growing vector-borne in US (May – November)
          o Separating false-positive Ab tests from asymptomatic infection is near impossible
     Prognosis
          o Definitive statements regarding outcome of Lyme Disease is difficult because:
                 (1) the inability to separate false-positive titers from asymptomatic infection
                 (2) the necessity of depending on clinical acumen in diagnosing erythema migrans
                     (titers are often negative at this early stage of infection)
                 (3) the lack of uniform treatment regimens
                 (4) the absence of long-term follow-up in most patients.
          o Approximately 80% of untreated or inadequately treated Lyme Disease patients develop
             some manifestation of disseminated disease.
                 Episodes are typically sub-acute and transient.
       o Patients with neurologic disease who are not diagnosed and treated early and aggressively
           can develop persistent neurologic and cognitive dysfunction that is more difficult to treat
           and often unresponsive to antibiotics.
                Cranial nerve palsies usually resolve without treatment but other neurologic
                   symptoms may take 6 months to reach maximum improvement
       o Patients with cardiac disease (A.V. blockade, arrhythmia's, syncope) rarely exhibit chronic
           morbidity from their heart involvement.
       o Some genetically predisposed individuals with arthritis may have ongoing joint
           inflammation that is not responsive to antibiotic therapy.
       o All outcomes appear to be improved by initial treatment with doxycycline or amoxicillin.
       o Bilateral Bells palsy =
       o TREAT…DO NOT TRUST TITERS!!! ****
   Post Lyme Syndrome
       o Data does NOT support Post-Lyme disease syndrome (anecdotally, 15-55% of pts report
           some degree chronic intermittent symptoms
       o Sx: cognitive disturbance, fatigue, joint/muscle pain, headaches, hearing loss, vertigo, mood
           disturbances, parasthesias, difficulty sleeping
       o Criteria: fatigue, MSK pain, and/or cognitive difficulties within 6mo after completion of
           antibiotic therapy
       o NO evidence says prolonged antibiotics will help
   Prophylaxis
       o Some say oral antibiotics if bite is engorged or if pt is pregnant
       o Degree of engorgement was an important variable in transmission of disease
       o FEMALE nymph causes it
       o Pro dose: 200mg doxycycline recommended if
                The attached tick can be recognized as I scapularis (adult or nympha), and it is
                   estimated to have been attached for more than 36 hours.
                Prophylaxis can be started within 72 hours of the time the tick was removed.
                Doxycycline is not contraindicated.
                Prophylactic antibiotics are not recommended in pregnant women
   Vaccine
       o 1998: Vaccine – LYMErix (recombinant OspA) against outer surface protein A of B. burg
       o 2002: withdrawn because wasn’t making money
   Diagnosis
       o 25-30% recall being bitten by nymph (small and painless)
       o Erythema migrans!!
       o Reinfection is very common! Relapse unusual if tx with appropriate antimicrobials
   Stage 1: Early localized (1-30 days post infection)
       o Isolated erythema migrans, undifferentiated febrile illness
       o Erythema migrans generally asymptomatic (axilla, groin, popliteal areas)
                Will go away in 2-3 weeks.
       o Pt with erythema and mild illness = Lyme’s; worse sx = more acute infection with Lyme’s
       o 1/3 all patients with erythema migrans will resolve on their own
       o Other sx: fatigue, myalgia
       o Co-infection!
   Stage 2: Early disseminated LD (weeks to months after bite)
       o 1 or more organ systems involved as hematologic or lymphatic spread disseminates
           spirochetes to distant sites
       o Direct and immunologic reactions account for patho, Signs/sx
       o MSK and neuro sx are most common
       o Intermittent inflamm arth begins as migratory polyarticular process involving bursa,
           tendons, joints which evolves 1-2 days  monoarticular process of knee, ankle, wrist
       o 2/3 of pts: first episode occurs within 6mo of erythema
       o Untreated: last 1-3months
       o Recurrences likely to involve more than 1 joint than initial event
       o Neuro involvement: Lyme neuroborreliosis in 5-20% cases
                Cranial Nerve 7 most common manifestation
                Bilateral facial palsy seen in 1/3 pts and is rare***
       o Peripheral neuropathy (stocking and glove) fairly common, come-and-go
       o Peripheral finding: decreased vibratory sensation of distal lower extremities
       o When meningitis occurs, symptoms occur 2-10 wks follow infection
                Borrelia encephalopathy = mild confusional state; depression and irritability also
       o Most common cardiac abnormality: AV block  dizziness, syncope, dyspnea, chest pain,
   Stage 3: Latent Lyme disease (months or years later)
       o Refers to manifestations, primarily rheumatologic and neuro, that occur months to years
           after initial infection
                Neuro: CNS/PNS
                KNEE JOINTS
                Consistent with fibromyalgia
       o Typical: subacute encephalopathy, chronic progressive encephalomyelitis (RARE) and late
           axonal neuropathies
                Myelitis, when present, manifest hemiparesis, ataxia, seizures, cognitive
                   impairment, bladder dysfunction, hearing loss
       o Monoarthritis, joint symptoms
       o Last ~3 months and most often in knee or temporomandibular joints
       o The severity of joint involvement can range from intermittent episodes of subjective pain
           to destructive arthritis or chronic erosive synovitis.
       o Migratory oligoarthritis involving the small or large joints can occur throughout the body.
       o Acrodermatitis chronica atrophicans develops during this phase
       o Females, especially older patients, tend to be more commonly affected.
       o Acrodermatitis chronica atrophicans tends to occur acrally, especially on the dorsal
           surfaces of the hands, feet, knees, and elbows.
   Lab Testing
       o CDC/Sed rates normal, Ab titer normal in early stages (6-8 weeks to show up)
       o Erythema migrans should be treated w/o waiting for results!
       o CDC: 2-step testing procedure with ELISA or immunofluorescent assay followed by
           Western immunoblot test on any samples with positive or equivocal results on ELISA
                The first step in patients with symptoms consistent with Lyme disease is to obtain
                   an antibody titer.
                        This can be either a total Lyme titer or separate immunoglobulin G (IgG) and
                            immunoglobulin M (IgM) titers.
                The second step is to confirm positive titers with a Western blot.
   CSF Testing
       o Lyme disease produces a pleocytosis characterized by mononuclear cells.
       o Spinal fluid levels of IgM and IgG antibodies to B burgdorferi should be measured, and an
          index of cerebrospinal fluid (CSF) to serum antibody (immunoglobulin-to-albumin ratio)
       o CSF cultures are positive in less than 10% of patients with apparent meningitis, intrathecal
          antibodies and a lymphocytic pleocytosis (approximately 100 cells/µL) are present in more
          than 80%.
       o Patients with meningitis secondary to B. burgdorferi typically have elevated protein
          concentrations (>50 mg/dL) but normal glucose levels (45-80 mg/dL).
       o Oligoclonal bands specific for B burgdorferi may be present.
       o A positive Lyme disease serology in CSF does not mean that the person has
               IgG and IgM antibodies may persist in CSF long after adequate treatment and in the
                 absence of evidence of active neurologic disease.
   Management
       o Outpatient antibiotics
       o Only cutaneous manifestations: no hospitalization
       o Carditis: hospitalization to prevent syncope during AV block (antibiotics, maybe
       o Chronic arthritis that doesn’t respond to antibiotics  synovectomy
       o Prior to surgery, NSAIDs and DMARDs like HCQ
       o Antibiotic Tx
               Doxycycline, amoxicillin, or cefuroxime axetil for 10-14 days is indicated for
                 early localized or early disseminated disease associated with erythema
                 migrans in the absence of neurologic involvement or third-degree heart block.
               Macrolides are alternative agents, but they are used only when the first-line agents
                 are not tolerated or are contraindicated. (not good for bone or CNS)
               Lyme disease arthritis without neurologic disease may be treated orally for 28 days.
                      Retreat for 30 days with an oral regimen or intravenous ceftriaxone if the
                        first oral course is unsuccessful.
                      If synovitis persists after a second course of antibiotics, hydroxychloroquine
                        has been shown to be effective
               The duration of the oral regimen for acrodermatitis chronica atrophicans is 21 days.
               Oral doxycycline may be as efficacious as parenteral antibiotics in patients who have
                 Lyme-associated meningitis, facial nerve palsy, or radiculitis.
               An oral antibiotic regimen for 30 days is indicated for those with facial palsies.
                      Although facial palsies may resolve without treatment, antibiotic therapy
                        may prevent further sequelae
               Evidence from multiple (3 ) controlled trials demonstrate a lack of benefit
                 from prolonged antibiotic treatment of what is known as post-Lyme syndrome
                 (symptoms persisting or recurring after appropriate treatment in the absence of
                 evidence of ongoing infection)
               The treatment of fibromyalgia and fibromyalgia like symptoms following
                 Lyme disease has not been shown in any controlled trials to be responsive to
                 antibiotic therapy.
                      A study by Klempner et al failed to show a benefit of treatment with 2 g of
                        intravenous ceftriaxone daily for 30 days, followed by oral doxycycline at
                        200 mg/d for 60 days.
   Controversy Surrounding Latent
       o No evidence of antibodies working for chronic Lyme syndrome
Limping Adolescent – Hip Joint
    Gait: 40% swing phase, 60% stance phase
         o Antalgic gait: gait that changes in response to injury or pain (less time on injured limb in
             stance phase, with more time in swing phase)

      Case 1: 8-year-old Little League baseball player presents with 6 month history of limping. Only
       recently has he had pain; pain is achy, gradual onset, without trauma, is worse during baseball
       practice and is now present with all activities.
          o Review of Systems: No history of illness. No fever or constitutional symptoms (weight loss
              or failure to thrive)
          o Hx
                   Onset and duration
                   Association with pain
                   Getting better, worse, or staying the same?
                   Location of pain (referred patter??)
                   Worse in the morning? (suggests rheumatologic process)
                   Worse at night? (pain that wakes a child from sleep  malignant process)
          o PE: Appears in good health, afebrile. Appropriate ht and wt for age. Inspection: antalgic gait
              favoring left; no gross deformities in legs or hips. No atrophy of thigh muscles. Palpation:
              tender over the entire left hip. ROM: IR and hip Abduction restricted and caused significant
              pain. Decrease ROM in abduction, IR, and flexion. (Asymmetric)
      Growing pains: diagnosis of exclusion
          o Often bilateral leg pain
          o Pain occurs ONLY AT NIGHT
          o No limp, pain, or symptoms during the day
      Bone growth
          o Formation from hyaline cartilage. Chondrocyte makes cartilage, develop growth plate. In
              adult bone, epiphyseal plate gets calcified. Secondary ossification centers develop, which
              add bone to hyaline cartilage scaffold as growth occurs and increased strength is required.

       o Embryology and Femoral-Acetabular Development: Hip joint begins at 7th weeks.
          Differentiates into femoral head and acetabulum by 11th week gestation. Between months
          4-7 of life, proximal femoral growth plate appears. Growth of proximal femur affected by
          muscle pull, transmitted hip joint forces (weight bearing), joint and systemic nutrition,
          circulation, muscle tone.
   Femoral Head Blood Supply
       o In utero, femoral head supplied from metaphyseal vessels, lateral epiphyseal vessels
          running in retinaculum up the femoral neck; little supply from ligamentum teres.
          Metaphyseal vessels decrease around age 4, but ligamentum teres doesn’t mature until age
          7. Between 4-7, femoral head entirely dependent on lateral epiphyseal vessels. These
          vessels lie within the hip capsule and are susceptible to external compression from intra-
          articular effusion.
   Legg-Calve-Perthes Disease
       o Idiopathic osteonecrosis of proximal femoral epiphysis (usually secondary ossification
       o “Coxa plana” – Calve described Xray findings of hypertrophy of femoral head, increased
          density, flattening and fragmentation of epiphysis.
       o Stats
               Frequency: 1/1200 < 15years
               Mortality: Self-limited if not treated, outcome Extremely variable
               Sex: Males>Females (4-5:1)
               Age: usually 2-12years; most 4-8years
               Race: Whites more affectes (family hx in 10%)
       o Pathology
               Etiology unknown. Capital femoral epiphyseal blood supply interrupted
                  (hypercoagulability and decreased venous outflow).
               Bone infarction occurs: AVN of subchondral cortical bone and 2o ossification center.
                  Articular cartilage continues to grow and thicken because it nourished by
                  synovial fluid. Temp cessation of epi growth, usually 6-12months.
       o Waldenstrom’s Pathologic Stages
               Stage 1: Initial phase (6mo)
                        Character: Synovitis, Joint irritability, Early necrosis of femoral head
               Stage 2: Bone fragmentation and Resorption
                        Revascularization occurs from periphery. Increased blood flow leads to
                          invasion and resorption of necrotic bone, leaving cystic areas and isolated
                          areas of bone. Femoral head becomes cystic- seen in xray findings.
                        If subchondral fracture occurs, patients develop LCP
                        Normal stress transmitted to femoral head cause fracture of weakened
                          necrotic bone; changing femoral head structure.
                        Fracture of necrotic subchondral trabeculae produces a tangential line on
                          radiographs: Crescent / Salter / Caffrey's sign
                        Bone resorption at the superolateral femoral head forms a lytic “V” (rat
                          bite): Gage's sign

         Stage 3: Reossification/Resolution
              Praphyseal ossification – reossification begins at margins of epiphysis
              Distortion of femoral head may occur. Coxa magna develops with growth
                 arrest of femoral neck. Abnormal stresses transmitted to growth plate may
                 cause distortion or growth arrest. Femoral head has poor bone strength and
                 may collapse. Lateral portion of head becomes uncovered.

                                       “Uncovering” of lateral femoral head

                                   Coxa Magna

                  Gage’s Sign
o LCPD Patho: new, normal bone replaces dead bone. Either good outcome, or early DJD.
o LCPD Hx: Symptoms present for weeks because child often doesn’t complain.
      May be painless at first, then hip or groin pain; may be referred to the medial thigh
        or knee.
      Mild or intermittent pain in anterior thigh or knee
         Limp - often painless and intermittent
         Usually no history of trauma
o   DDx: ****ON TEST****
         Bilateral Perthes: (requires skeletal survey work up)
                hypothyroidism
                sickle cell anemia -15% have femoral head AVN
                multiple epiphyseal dyspasia
                spondyloepiphyseal dysplasia tarda (Collagen Type II Defect)
         Unilateral Perthes:
                septic arthritis
                transient synovitis
                sickle cell
                spondyloepiphyseal dysplasia tarda
                gaucher's disease
                eosinophilic granuloma
o   PE:
         Antalgic gait
         Short stature: Children with LCPD often have delayed bone age.
         Inspection:
                Atrophy of thigh muscles secondary to disuse
                Leg length inequality due to collapse
         Palpation:
                Muscle spasm
                Thigh atrophy
                 thigh circumference on the involved side due to disuse.
         Galleazi Test: suggesting developmental dysplasia of hip or leg-length discrepancy.
           Test positive when knees are at different heights as pt lies supine with ankles to
           buttocks and knees/hips flexed.
         Range of Motion (ROM):
                 range of motion with internal rotation and abduction
         Roll test
                With patient lying in the supine position, the examiner rolls the hip of the
                  affected extremity into external and internal rotation.
                This test should invoke guarding or spasm, especially with internal rotation
         Catterall's sign
                passive hip flexion causes external rotation. (sensitive; not specific)
o   Tx: Early Diagnosis (most important)
         Place the femoral epiphysis within the acetabulum & maintaining abduction and
           internal rotation reduces forces on the epiphysis, allowing it to remodel.
                Without containment, the femoral epiphysis deforms & extrudes from the
                  acetabulum; particularly if the hip maintains adduction & external rotation.
         Scottish Rite Abduction Orthosis
o   Poor Prognosis
         Clinical: sex, progressive loss of movement, adduction contracture, flexion w/
           abduction, heavy childe, age (better younger than 8)
         Radiological: head partially uncovered (most important), percentage of femoral
           head involved (more = worse), calcification lateral to epi, metaphys cysts, Gage’s
           sign, horizontal physis
o   Outcomes: most pts have good outcome. DJD related to earlier age of onset.
   Case 2: 4 year old boy brought in by his mom presents with fever to 101 and a 2 day history of not
    walking. At first he complained that his hip hurt, and then was limping. He recently was home
    from school due to an illness about 10 days ago.
       o On exam: He appears uncomfortable but well. He has no fever. He has pain in the hip and
            anterior groin with any motion. There is no rash. There is mild anterior adenopathy.
   Transient Synovitis (self-limited benign condition which can resemble LCPD)
       o PTS PRESENT WITH PAIN AND LIMP: anteromedial aspect of thigh and knee.
       o Hx of recent URI
       o ROM: leg often held in flexion and slight ER.
       o Blood tests normal
       o Radiographs: capsular bulging; no bony changes r/o AVN
       o 1.5% WITH TS DEVELOP LCP
       o Usually resolves in 1-2wks (marked improvement 24-48hrs)
       o Tx:
                Bed rest 7-10 days; no weight bearing on affected limb
                NSAIDs
       o Recheck Xray
                2-3 months
                if symptoms persist >2wks (r/o LCPD)
   Case 3: A 10 year old comes in with his mother, who states he has had a 1 day history of fever to
    102.8o and limping with pain in the right hip. He has used some Tylenol® for the pain.
       o On exam: He appears sleepy. His temperature is 101.9o resp 20, pulse 105. He will not
            bear weight. There is redness and swelling around the right hip. The hip is painful with
            any ROM. Sensation is normal; there is marked adenopathy.
   Septic Arthritis
       o Kids appear “sicker”
       o Higher Fever
       o  WBC and ESR (sed rate)
       o Needs rapid diagnosis to avoid damage to articular cartilage
       o Can pre-dispose to LCP disease – capsular pressure
       o Antibiotics/surgical drainage
       o Treatment needs to be rapid
                Antibiotics, surgical drainage
   Case 4: 16 y/o WM football player with 5 days of severe left knee pain. Spent summer playing 36
    holes 3x/wk. After teeing off on 2nd tee of 2nd round, he had sudden onset left knee pain. Pain is
    sharp, over medial aspect. Severe enough that he is unable to finish; walks with a severe limp.
    Pain is better when reclining with knee supported.
       o PMH: Injured his knee 4 years ago playing football and has worn a knee sleeve since. This
            pain is similar pain.
       o Exam: prefers flexion and abduction/ER
       o Vitals normal
       o Knee exam
                Right leg in ext rotation; right leg 1 cm shorter than left.
                Full Range of Motion (ROM)
                Strength: Right quad atrophy
                Stability: normal MCL, LCL
                Cannot position leg for ACL
   SCFE: Slipped Capital Femoral Epiphysis
       o Among most common adolescent hip disorders
o Patient may complain of hip, medial thigh, and/or knee pain
o Acute or insidious onset of limp,  range of motion.
o Instability of the proximal femoral growth plate.
o On x-ray, the femoral head displaces posteriorly & inferiorly in relation to the femoral neck
  within the confines of the acetabulum.
o Histology: SCFE is a physeal fx. In SCFE, epi growth plate unusually widened, due to
  expansion of zone of hypertrophy. Abnormal cartilage maturation occurs leading to
  disruption of normal cartilaginous palisading architecture. Slippage occurs through
  weakened area.

o Clinical Classification
       Acute : symptoms (e g, hip or knee pain, limp, decreased range of motion) for
          less than 3 weeks
       Chronic: symptoms greater than 3 weeks are termed chronic.
       Acute on chronic: symptoms > 3 weeks but presents with acute exacerbation of
          pain, limp, inability to bear weight, or  ROM with or without an associated
o Classification schemes
       Acute vs. chronic vs. acute-on-chronic
       Stable or unstable – stable can bear weight, unstable can’t
       Radiographic (Type I, II, III)
o Complications
       AVN of the femoral head
               Risk is 20-50% with an attempted reduction vs < 5% without reduction.
       Chondrolysis
               Destruction of cartilage is believed to occur irrespective of the method of
       Leg length discrepancy
               from incomplete reduction, AVN, chondrolysis, or secondary coxa vara.
       Hardware failure
       Failure of epiphysiodesis,
       Slip progression
       Infection
       Osteoarthritis - late complication
               From AVN, chondrolysis, or alterations of hip biomechanics
o Imaging: Xray, AP/ Frog-leg
o Tx:
       Prevent further slippage
       Reduce Osteonecrosis
               Higher risk in acute and unstable slips.
               Less with single screw fixation.
                    Reduce Chondrolysis.
                    Growth plate closure
                         Condition stabilizes once growth plate is closed; no further slippage
                         Bone-graft epiphysiodesis (closure of growth plate) may be performed if
                           patient age permits
                  Boys<12.5; girls<10.5 yr.
                    Diagnosis
                    Surgical fixation
                         Allows early stabilization of the slip, enhancement of physeal closure,
                           prevention of further slippage,  symptoms with minimal morbidity.
                         Usually pinned in-situ, but gentle reduction sometimes attempted

Non Traumatic Foot and Ankle Pain
    Hx
         o HPI
                 OLDCARTS
         o Previous injury
         o Previous surgery
         o Meds
         o Allergies
         o SH – work status
         o FH
         o ROS
    DDx
         o Bone
                 Stress/fracture medial maleolus, talus, navicular
         o Ligaments, fascia
                 Spring ligament, plantar fasciitis
         o Nerve
                 Posterior tibial nerve entrapment
                 tarsal tunnel syndrome
         o Tendon
                 Tibialis posterior, flexor hallucis, flexor digitorum
         o Somatic dysfunction
                 Arch dysfunction – cuneiform, navicular, talus
    Foot Type
         o Arch type determines where stresses are transmitted
                 Pes cavus – high arch
                 Pes planus – low arch
    Functional Arches of the Foot
         o Lateral Longitudinal Arch
                 calcaneus, cuboid, 4th and 5th MTs
         o Medial Longitudinal Arch
                 calcaneus, talus, navicular, cuneiforms and 1st three MTs
         o Distal Metatarsal Arch
                 articulations of the metatarsal heads with the phalanges
         o Proximal Transverse Arch
                 cuneiforms and the cuboid
    Medial Longitudinal Arch
         o Tibialis anterior increases arch
       o Tibialis posterior eccentrically contracts to preserve arch
       o Longitudinal muscles prevent separation of bone
       o Keystone shaped bones – can roll in or out
       o Strut ligaments (spring ligament)
   Functional Arch Assessment
       o Inspection
       o Functional: forward squat test, have pt squat keeping heels on ground, assess arch
           pronation (arch rolls medially) as well as heel cord tightness.
       o Heel shape: Varus – supinated, Valgus – pronated
   Always assess gait: look for limp or dysfunctional gait
       o Watch alignment of hips, knees, ankles
       o Watch for how weight is transferred and dysfunctional muscle firing patterns
   Case 1: A 44 year old patient is overweight and has decided to get into shape. She started a
    walking program of 2 miles a day 4 weeks ago. About 3 weeks ago, she developed pain which
    begins in her arch and radiates up the medial aspect of her leg. She notices the arch has
    dropped and it is swelling; she is starting to limp.
   Posterior Tibial Tendinitis
       o Typical pt: 35-58yo woman who begins exercise program
       o Complains of progressive, achy pain in medial arch
       o PE: pain with posterior tibialis MMT, unilateral pronation on forward squat test
       o Work-up: Xray
       o Tx:
                Cast or booth with orthotic x3-4wks, reproduce arch, then PT
                Surgical consult
                Significant risk of DJD with rupture
   Arch Pain and Deformity
       o Ligament stretch and distortion of the arch of the foot
       o Loss of structure leads to loss of function
       o Causes pain and (over time) degeneration of bone and joint
       o SCS, ME, HVLA techniques can help restore normal structure
   Case 2: Patient complains of pain in the posterior aspect of the calf near the ankle over last 6
    weeks. Pain is progressive with swelling in the posterior aspect of the leg just proximal to the
    heel. One-sided.
       o It is associated with pain when pushing off during running and with “stair stepper” at
           work. Pain is worse with exercise, 5/10 stiff achy pain. In the morning she wakes up stiff
           and it hurts the first steps out of bed.
   Anatomy for Differential Diagnosis
       o Haglund’s Deformity (AKA “pump bump”), retrocalcaneal bursitis
       o Os trigonum/impingement
       o Insertional tendinitis
       o Retrocalcaneal fat pad
       o Severe’s Disease: apophyseal traction in pts with open growth plates
       o True Achilles tendinitis
       o Somatyc dysfunction
   Tendon structure
       o Misnomer: a true tendinosis, secondary to overuse – particularly eccentric overuse
       o Anatomy: tendon, paratendon
       o Histopath: geneneration and disorder of collagen fibers, increased vascularity, “mucoid”
           collagen degeneration
                   Repetitive eccentric overuse overwhelms ability of fibroblasts to repair damaged
                 Steroid injections inhibit fibroblastic activity (assoc with tendon rupture)
   Achilles Tendinitis
        o Pain at post heel, prox to calcaneus
        o Insidious onset (stiff with running, in AM)
        o Swelling, nodule, both (migrates with flexion, like Achilles)
        o ~18% runners
        o risk factors: age, cavus feet, tibia vara, heel and forefoot varus; overuse/jumping
        o Tx:
                 Stretching of gastroc and soleus
                 eccentric exercise a potent stimulus for linear collagen matrix formation and
                    recovery from tendinosis
                 somatic dysfunction?
   Achilles Tendon Rupture
        o “complication”
        o Hx of activity with sudden pop
        o Fluoroquinolone use
        o Dx: Thompson test (squeeze calf, should see plantar flexion), MRI
        o Tx: Surgical repair
   Case 3: 45 year old complains of heel pain, medial plantar surface of the calcaneus (heel), worse
    the first steps out of bed in morning. Gradually getting worse since started 2-3 months ago.
        o DDx
                 Fat pad syndrome (calcaneus tilted, so more WB at bony part of heel)
                 Plantar fasciitis
                 Foreign body
                 Medial plantar nerve entrapment
                 Bone bruise/stress fracture/fracture
   Lateral Plantar Nerve Entrapment
        o Lancinating pain that radiates
        o May persist at rest
        o Tinel’s sign at lateral plantar tunnel reproduces pain
        o Conservative: surgical alternative
   Plantar Fasciitis: NOT heel spur
        o Morning sx related to fascial tension
        o Pain at medial insertion
        o Windlass maneuver
        o Medial and middle cuneiform bones
   Case 4: 26 year old complains of “shooting” foot pain that is on the dorsum of her forefoot and
    goes to her toes. It started after dancing a few weeks ago and now is worse when she wears
        o DDx:
                 Any site: stress/true fx, tendinits, infection, tumor, synovitis
                 Metatasal:
                         Metatarsalgia
                         Interdigital Neuroma
                         Turf Toe
                         Sesamoid pathology
                         Friedberg’s infarction
                               o Avascular necrosis of the second MT head - possibly following trauma
   Morton’s Neuroma: fibrosis of perineural area of common digital nerve leads to entrapment
       o Primarily btw 3 and 4 MT
       o Sharp, stabbing, lancinating pain
       o Worse when wearing shoes (women>men, toe box size)
       o Proximal to transverse intermetatarsal ligament
       o Dx
                Clinical
                Palpation of distal intermetatarsal spaces
                Mulder’s sign: pain with compression of MT heads laterally. Relieved by plantar
                   pressure directed dorsally
                Laseague’s sign
       o Work-up: Xrays to look for osteophytes or masses in MT heads that could compromise
           interdigital nerve space
       o Tx: Conservative – neuroma pads, icing after exercise, orthotics or arch taping, NSAIDs,
           larger toe box, injection
   Case 5: 45 year old factory worker complains of dull achy dorsal foot pain while walking. Has
    gotten worse over months. At first only while working, but now at night. Now he is limping.
       o “March” Fx
                ~90% of all metatarsal stress fractures
                Occurs at the neck of the 2nd, 3rd, and 4th
                Especially common in runners
                Dancers have similar history and pain in 1st MT
                Work up: Xrays
                       50% will be negative
                       Bone Scan
                Treated with stiff-shoe for 4-6 weeks
   Common site for stress fx: 4th MT
   Which stress fx has complications? 5th MT
   Fx Zones
       o Zone 1 – avulsion injury; involves metatarsocuboid joint (93%)
       o Zone 2 – metaphyseal-diaphyseal junction, always an acute fracture - true Jones Fracture
       o Zone 3 – stress fracture of proximal 1.5 cm of shaft; always have prodromal symptoms or
           radiographic signs of ongoing stress (3%)
       o Dx
                Clinical Suspicion
                X-rays
                       Usually negative
                       Periosteal reaction
                Bone Scan
                       Demonstrates areas of high bone turnover
                MRI shows bone edema
       o Tx
                Phase I – modified rest
                       Pain control
                       Brace/stiff-shoe/cast – limits motions
                       Muscular strength & endurance
                       Stretching and flexibility
                       Maintaining fitness/Cross-training
                Phase II – gradual reintroduction of sport
                             Cont Phase I objectives
                             Risk factor modification
                             Biomechanical factors, orthotics, OCPs, calcium, bracing
                             Metabolic and nutritional factors
     Sesamoids
         o Pain under the ball of the foot
         o Can be injured during running, jumping – Direct impact
         o Injuries
                  Sesamoiditis – bone bruise
                  Stress vs true fracture vs bipartite sesamoid
         o Typically medial is most involved
         o Exam
                  Pain on palpation
                  Pain on plantar 1st MTP joint.
                  Pain with maximum dorsiflexion 1st ray
                  Inability to push-off
     Bunion – Hallux valgus
         o Valgus deformity at 1st MTP joint
         o Associated with shoes with tight toe box
         o Treatment
                  Orthotics
                  Wide toe box
                  Surgery after conservative measures fail
                  OMT/Somatic dysfunction?
     Hallux ridges
         o Degenerative joint changes at first metatarsal-phlangeal joint (MTP) – older patients
         o Limits first MTP joint dorsiflexion
         o Important consideration in geriatric gait assessment
         o Diagnosis by palpation, examination, and x-ray

Surgical Tx of Knee Injuries
     PE:
            o   Observation
            o   Range of Motion (ROM)
            o   McMurray’s
            o   Apley’s Distraction and Compression
            o   Squat
            o   Varus and Valgus Stress
            o   Anterior and Posterior Drawer
            o   Lachman’s
            o   Slocum Anterior Rotary
            o   Lateral Pivot Shift

   Note: Blood supply is limited to some zones…”Zones of Vascularity”

   Knee aspiration: parallel to distal anterior femoral shaft
   Meniscal Tear:
       o MOI: Twist w/ WB
       o S and S: Pain along joint line, clicking, locking, mild swelling, vague aching throughout day
       o Tx: depends on size of tear; PT successful in ½ of cases (tear will smooth out BUT NOT
          GROW BACK)
       o Arthroscopy: most common procedure
   ACL Tear
       o Deceleration or cutting, “pop” and fall, swelling w/ in a few hours, 70% likelihood of ACL
       o Lachman’s most sensitive test
       o Segond – pathognomonic
       o Meniscal injuries – 50-75%
       o Osteochondral injuries – 30%
       o Blood supply
       o TX:
              Nonoperative vs. operative (OPERATE. If not, there will be cartilage damage)
              Associated injuries

   ACL Reconstruction
       o Options: Patellar Bone- Tendon- Bone (PBTB)
       o Hamstring
       o Autograft vs. allograft (chance of viral transmission, but very small)
       o Screws between tunnel and bone plug. Common mistake is not putting tension of graft and
          screw pushes bone into joint, causing laxity of that repair
       o Complications
               Patellar fx.
               Inadequate graft length
               Bone plug – hole mismatch
               Graft fracture
               Suture laceration
               Violation of post. femoral cortex
               Incorrect tunnel placement
               Extension lag
               Persistent anterior knee pain
               Loss of ROM
   PCL Tears
       o Fall on flexed knee or dashboard injury, many asymptomatic at first
       o Post Drawer indicative, but beware of starting tibial position
       o Sag test
       o Stress radiography – 8mm +
      o MRI Best
      o Tx: Non operative vs. operative? (controversy: doctor’s may not be comfortable because it’s
          not as common, and people with these tears have little disability)
   Complications of PCL Reconstruction
      o Inadequate graft length
      o Bone plug – hole mismatch
      o Graft fracture
      o Suture laceration
      o Violation of post. femoral cortex
      o Incorrect tunnel placement
      o Flexion lag
      o Neurovascular injury
      o Osteonecrosis of medial femoral condyle

   Collateral Ligament Tears
        o Operative vs. nonoperative??
        o Pt demands
        o First, second , third degrees
        o Assoc injuries?
        o MCL – nonoperative more successful if tear is proximal
        o ACL – many treat only ACl and treat MCL conservatively
        o LCL not as well researched
   OA: surgery may be indicated for “temporizing” measures (i.e., can’t have replacement until next
        o Debridement for knee OA usually ineffective
   Osteochondritis dissecans (OD)
        o Most common cause of loose bodies in knee
        o Etiology: ? ischemia, rep micro-trauma, hereditary, and others
        o More common in adolescent males
        o Vague, aching discomfort
        o Medial femoral condyle
        o Hx of trauma in 40-60% of pts
        o PE – tender over lesion
        o TX: depends on pt age and degree of involvement
                Conservative care
                Drilling or excising fragment
                Debridement of crater
                Pinning with pins, “cortical matchstick”
                Most commonly used open techniques:
                     Removal of loose bodies
                     Curretage and drilling of crater
                     Replacement and pinning of fragment


   Summary!!!
       o MENISCAL INJURIES – McMurray’s, mechanical symptoms, arthroscopy
       o Meniscal mobility and vascularity (lateral moves better)
       o ACL - repair
       o PCL – depends on pt.
       o COLLATERAL LIGAMENTS – often treated conservatively
       o OA – arthroscopic debridement not helpful
       o OD – arthroscopy helpful, curretage, pinning
       o Interpret radiographs of OD, and MRI’s of Cruciate ligament injuries
   Terrible Triad: ACL, meniscus, LCL
Joint Replacement
     Knee has 3 compartments: 1st(medial), 2nd(lateral), 3rd (patellofemoral joint)
     Signs of OA
           o Loss of joint space
           o Sclerosis
           o Osteophytes
           o Osteopenia d/t disuse

      1 compartment
           o Loss of joint space, sclerosis, osteophytes, osteopenia

      Types of Knee Replacement Arthroplasties
          o Tricompartmental (“Total Knee,” TKRA)
          o Unicondylar Knee Arthroplasty (“Uni,” UKRA)
      Indications for TKRA
          o Relieve pain caused by severe arthritis, whith or without significant deformity
                  Conservative measures: anti-inflamm, activity modification, injection, use of cane
                  Differential: Sciatic irritation, referred pain from ipsilateral hip, PVD, meniscal
                     patho, bursitis of knee try these first
                  Imaging: if cartilage space not completely lost, pts less satisfied post-op
                  Finite expected survival adversely affected by activity level
          o Younger patients with systemic disease and multiple joint involvement
          o Deformity: progression begins to threaten expected outcome of arthroplasty.
      Absolute Contra-indications to TKRA
          o Recent or current infection
          o Remote source of ongoing infection
       o Extensor mechanism dysfunction
       o Recurvatum secondary to muscular weakness
       o Painless, well-functioning arthrodesis
   Relative contra-indications to TKRA
       o Medical conditions
       o Ability to undergo significant rehab
       o Atherosclerosis of operated leg
       o Skin conditions
       o Venous stasis disease
       o Neuropathic arthropathy
       o Morbid obesity
       o Recurrent UTI
       o Hx. of osteomyelitis
   Leave patellar un-resurfaced at time of TKRA if:
       o 1.Primary diagnosis of osteoarthritis
       o 2. Satisfactory patellar cartilage with no eburnated bone.
       o 3.Congruent patellar tracking
       o 4.Normal patellar shape
       o 5.No evidence of crystalline or inflammatory arthropathy
       o extensor mechanism problems are not uncommon complications
   High Tibial Osteotomy (HTO) “rotating the tires” – allows pt to use “own” equipment for a longer
       o Motivation for procedure
                Narrowed medial cartilaginous space may regenerate (and associated degenerative
                  features may reverse) if weight bearing stresses are partially shifted from the
                  medial to the lateral side of the knee (shifting the mechanical axis from relative
                  varus to valgus);
                Results of osteotomy about the knee are most dependent on the limb alignment and
                  joint line inclination after surgery
                In a varus knee w/ medial unicompartmental DJD, correction to 8-10 deg of
                  anatomic valgus is associated w/ best prognosis while knees left w/ residual varus
                  have a less satisfactory result;
                Of note: several months need to elapse before the patient is fully mobile, & it is often
                  a year or more before the patient is free of pain;
                By contrast TKR gives almost immediate mobility & relief;
                To the elderly pt the advantage of replacement is obvious; YOUNGER PT ONLY

   Indications for UKRA
       o Elderly, thin individuals with unicomp DJD
       o Younger individuals with UDJD
   Contraindications
       o Inflammatory arthritis
       o Flexion contracture > 15 degrees
       o Pre-op ROM <90 degrees
       o Deformity >10degrees
       o Significant cartilaginous erosion in the opposite compartment
       o ACL deficiency
       o Exposed subchondral bone beneath the patella
       o Obesity-study @ 40 months, failure of 20% with BMI >32

   Indications for Bilateral Simultaneous TKRA
       o Contraversial!
               Hospital stay – longer rehab
               Expense – can reduce charges by 58%
               Blood loss – depends on study
               Greater degree of post-op thrombocytopenia
               Higher rate of PE and DVT
               Fat emboli – slightly increased
               Assess comorbidities and physiological age when considering procedure
   Complications of Knee Replacement Surgery
       o Thromboembolism
               DVT – overall prevalence after TKA=40-84%
               PE- asymptomatic 10-20%, symptomatic 0.5-3%
               Mortality – 2%
               Treatment – prophylaxis for 14d (6wks w prior hx.) mechanical, warfarin, LMW
       o Infection
               S.aureus, S.epidermidis, and Strep. species – most common bugs
               prophylaxis – first generation cephalosporin
               aspiration – standard for diagnosis
               Treatment
                        antibiotic suppression (rarely indicated)
                        debridement
                        resection arthroplasty
                    arthrodesis
                    one-stage or two-stage reimplantation
                    amputation
       o Periprosthetic Fx
             Supracondylar fx (.3-2%)
             Tx depends on type
                    I: undisplaced, prosthesis stable
                    II: displaced, prosthesis stable
                    III: unstable prosthesis w/ or w/o displacement

   Bilateral Hip DJD: cysts, sclerosis, osteophytes, diminished joint space

       o Acetabular cysts
   Forces Acting on the Hip
       o Abductor musculature: acts on lever arm from lateral aspect of the greater trochanter to
           the center of the femoral head
       o Body weight: load applied to lever arm extending from the center of gravity to the center of
           the femoral head
       o Load on femoral head = 3xBW

        o Actions that decrease joint reaction force: lots of things
        o Actions that increase joint reaction force: Valgus neck-shaft angulation (decrease shear
           across joint)
        o Charnley Concept – shorten the lever arm of the BW by deepening acetabulum and
           lengthen lever arm of abductors by reattaching osteotomized greater trochanter laterally
               Today, neither concept is used – preserve bone, no osteotomies
   Stress Transfer to Bone
        o Wolf’s Law : form follows function. Stress shielding.
               Materials – modulus of elasticity, stress in proximal third of cement mass
               Geometry and size– larger stems increase stiffness, weight borne by stiffer object,
                  hence stress shielding
               Fixation – Cement, vs. cementless, collar vs. collarless
        o Femoral side: material, geo, size of stem, fixation – all impact stress transfer
        o Pelvic side: cemented plastic vs. cementless metal backed cups
   Design and Selection of Total Hip Components
        o Selection based on
               Patient’s needs
               Anticipated longevity
               Level of activity
               Bone quality and dimensions
               Ready availability of implants and instrumentation
               Surgeon’s experience
        o Femoral Component
               Goal: restore normal center of rotation of femoral head determined by:
                       Vertical height (vertical offset)
                       Medial offset (offset)
                       Version of femoral neck (anterior offset)
               ROM and Neck size/shape
               Three types: cemented, cementless/porous, cementless/press-fit
        o Acetabular Components
               Cemented: all poly, good choice in low-demand, elderly pts
               Cementless: porous coated, initial fixation
               Polyethylene liner: >5mm, highly crossed linked poly
               Head sizes
               Metal-on-metal bearings:
                       high carbide cobalt-chromium alloy
                       polar contact w clearance of 100-200μm
                       “self-healing”
                       particle size smaller than poly and more numerous, malignancies??
               Ceramic – on – ceramic bearings: smoother, more scratch-resistant than metal; but
                  impingement between femoral neck and rim
   Resurfacing Arthroplasty
       o Femoral component: cemented, high carbide surface content cobalt-chromium
       o Acetabular: porous coated, press fit with thin metal liner
       o Ideal: <60yo, active, normal prox femoral anatomy, normal bone density
       o Drawback: extensile approach needed, more technically demanding
   Indications for THRA
       o Arthritis
       o          Rheumatoid
       o          Juvenile RA
       o Ankylosing spondylitis
       o Degenerative joint disease
       o          primary
       o          secondary
       o Osteonecrosis
       o Pyogenic arthritis
       o Tuberculosis
       o Congenital subluxation or dislocation
       o Hip fusion
       o Failed reconstruction
       o Bone tumor involving prox. Femur
       o Hereditary disorders (e.g.,achondroplasia)
   Contra-indications
       o Absolute
               Active infection of hip or other region
               Any unstable medical illness
       o Relative
               Any process destroying bone rapidly
               Neuropathic arthropathy
               Absence or relative insufficiency of abductor musculature
               Rapidly progressive neuro disease
   Complications
       o Mortality - @90days 1%primary, 2.5%revision
       o Hematoma formation
       o Heterotopic ossification – 10%
       o Thromboembolism – 50% w/o prohylaxis, fatal PE 2%
       o Nerve injuries (sciatic, femoral, obturator, sup.gluteal)
               0.7-3.5%
       o Vascular injuries
       o Limb-length discrepancy
       o Dislocation and subluxation – 3%
               approach, prior hx., component postioning
               Usually w/in first 3 mos.; later assoc. w recurrence
               Tx. – reduction under anesthesia, bed rest, brace
       o 9. Fractures
        o 10. Infection – 1-2%
        o 11. Trochanteric nonunion or migration
        o 12. Loosening – detected best with annual radiographs
        o 13. Osteolysis
     SUMMARY!!!
        o Recognize radiographs of osteoarthritis (DJD) of knees and hips
        o 3 vs. 1 compartment involvement
        o Indications, contra-indications and complications of TKRA and THRA
        o High tibial osteotomy – option for Unicompartmental DJD of knee
        o Incidence and Treatment of complications
        o Biomechanical forces at hip and hip design considerations

Seronegtive Spondyloarthropathy
     Spondyloarthropathies: family of clinically, epidemiologically, and genetically related inflamm
      diseases that primarily affect spinal and peripheral joints
     “Seronegative” refers to the lack of serum rheumatoid factors (IgM auto-antibodies to IgG) in
      patients with the spondyloarthropathies. Patients are RF negative.
     Characteristics
         o Inflamed SI joints; usually ascending and spondylitis (bony fusion) often follows
         o Assoc with peripheral, assymetric, oligoarthritis
         o Primary sight of inflammation is entheses (enthesitis). This distinguishes the disorder from
             RA, where primary sight is the synovium
         o May be sights of extra-articular inflamm (including eye, aortic valve, gastrointestinal tract,
             GU, and integument
         o Disease onset occurs in young adulthood
         o Strong familial tendency and a striking genetic assoc with HLA-B27 ( not used to diagnose
             disease )
         o Certain bacteria play important pathogenetic roles
     Disease States
         o Ankylosing spondylitis
         o Reactive arthritis (Reiter’s Syndrome)
         o Psoriatic arthritis
         o Enteropathic arthritis
     Pathogenesis
         o Genetic Factors: 20% with AS have first-degree relatives with same disease
                  In monozygotic twins, concordance 75% compared with lower with dizygotic twins
                  90% have HLA-B27 (not specific)
                  Pts with HLA-B27 have 100x risk to develop AS
         o Environmental Factors
                  Assoc with enteropathic and STD, but no definitive evidence yet
                  Reactive arthritis once considered sterile joint disease, but recent studies reveal
                    presence of bacteria (but not same as septic, where you culture bacteria from joint
                    space; septic is acute – one joint)
     Ankylosing Spond
         o Most common
         o Mostly in men
         o Onset between 20-40 years
         o Peripheral enthesitis is common
o Dx
          Hx: insidious onset of dull lower back pain with radiation to buttocks. Worse in
           morning, and usually has nocturnal component. Improves with activity. Possible
           family members with similar symptoms
          PE: Look for loss of lumbar lordosis, increased thoracic kyphosis, cervical flexion,
           decreased chest expansion with inspiration.
          Special Tests: SI inflammation
               Shober’s Test: for loss of lumbar flexion. No increase = (+)

                 Patrick’s Test used to ID acute sacroiliitis. Pain = (+)

                 Gaenslin’s Test used to ID acute sacroiliitis. Pain = (+)

o Next, look for evidence of entesitis, tenderness, and pain with passive ROM of ligamentous
       At Achilles
       Tendon of insertions of toes  “Sausage digit”
o Criteria (ON EXAM*****)
       Low back pain of at least 3mo duration alleviated by exercise, not by rest
                Restricted lumbar spinal ROM
                Decreased chest expansion relative to normal values for age and sex
                Also, radiographic changes
                NOTE HLA-B27 not in criteria
       o Xray 1st test of choice
                Sacroiliitis: joint space narrowing, articular sclerosis
                Spondylitis: annular calcification leads to “Bamboo spine”
                Obvious loss of lordosis
       o Extra-articular manifestations
                Constitutional signs are common (fatigue, anorexia, mild fever)
                ANTERIOR UVEITIS IS MOST COMMON extra-articular manifestation
                Urgent ophthalmology consult indicated
                Cardiac – aortic root dilatation, mitral root dilatation
                Pulmonary – late stage disease (Hilar fibrosis)
       o Lab test
                HLA analysis not specific, but NOT DIAGNOSTIC
                ESR, CRP (tests of inflammation) usually elevated…again, not specific
       o Tx: Pharmaco
                NSAIDs are first-line tx – rapid improvement is helpful to empirically diagnose AS
                SSZ has been effective
                Future: TNF blockers, Etanercept, Infliximab
   Reactive Arthritis
       o Aseptic arthritis triggered from an infectious agent outside of the joint
                Triad (though many have no clinical evidence of urethritis or conjunctivitis)
                        Arthritis
                        Urethritis
                        Conjuctivitis or Uveitis
                               o “Can’t see, pee, or climb a tree!”
       o Etiology
                Enteropathic infection (Shigella, Yersinia, Campylobacter, Salmonella)
                GI infection (Chlamydia, Ureaplasma)
       o Presentation
                Arthritis begins 1-4wks after acute infection
                Oligoarthritis/enthesitis usually of lower extremities (Dactylitis)
                Inflamm back pain
                Fever
       o Extra-articular
                Essential in making diagnosis: Conjunctivitis, Urethritis, Diarrhea, painless oral
                Circinate balanitis (painless reddened lesion around glans penis)
                Keratoderma blennorrhagica: lesions on soles of feet
       o Tx:
                NSAIDs for pain
                Antibiotics if caused by chlamydia (with urethritis); culture organism before
                   treating (if they have infectious diarrhea; will resolve on its own)
   Psoriatic arthritis
       o Arthritis occurs in 5-20% of people with psoriasis; psor comes first before arth
       o Presentation
                Asymmetrical oligoarth
                Symmetrical polyarthritis resembles RA, but should be RF negative
                  Arthritis mutilans most destructive form; bone resorption and telescoping of
                   fingers are characteristic
                Psoriatic spondylitis
                Predominant DIP joint involvement
                Nail changes
       o Radiography: DIP involvement “Pencil in a cup deformity,” erosive arthritis
       o Tx:
                NSAIDs and use disease-modifying agents later
   Enteropathic arthritis
       o Spondyloarthritis occurs in up to 20% of patients with diagnosed inflammatory bowel
           disease (IBD=Crohns and Ulcerative Colitis)
       o Crohn’s causes more arthritis than ulcerative colitis
       o Common presentations: Peripheral arthritis, Spondylitis
       o Peripheral arthritis of IBD
                Symmetrical swelling of knees, ankles, wrists
                Seldom results in deformities
                Strong correlation between arthritis and severity of bowel disease
                During periods of a bowel flare-up, arthritis may be the first sign
       o Spondylitis assoc with IBD (clinically indistinguishable from AS).
                NO correlation of spondylitis with activity of the bowel disease
       o TX
                Peripheral arth: aimed at controlling inflamm bowel disease
                Spondylitis: therapy is exactly the same as ankylosing spondy. TNF blockers will
                   treat the arthritis as well as IBD
   Practice Questions
       o 25yo male presents with low back pain for 12 wks. Pain improved with activity but not
           rest. Thinks it’s from heavy lifting. Asks for pain meds and work excuse. Most appropriate:
                Clarify more details about hx (before xrays, PT, medication, blood test)
       o After careful hx and pe, suspect they have AS. To confirm, must have all but
                HLA-B27
       o First line therapy for pts with reactive arth from GU
                Antibiotics
       o 25yo female med student with new onset arth. Asymmetric and oligoarticular affecting R
           knee and L ankle. No skin lesions. Next step?
                Take a sexual history (HISTORY always next step!! Before other tests)
       o 34yo male with Crohns and peripheral arth. First line tx
                tx of underlying inflamm bowel disease
       o 31yo male with low back pain of 5mo. Pain and stiffness in lower back worse in morning
           and improving with activity. Patrick’s test positive. Xray confirm suspicion of sacroiliitis.
           Blood confirms HLA-B27. What is not diagnostic?
                HLA-B27
       o First line for AS?
                NSAID
       o 24yo male med student returns from Vegas. Urethral discharge and arthralgias. Cultures
           positive for Chlamydia. Suspect joint pain from reactive arthritis. Diagnostic includes all
                Fever
       o Primary tx of reactive arth related to chlamydia
                Antibiotics to treat underlying infection
       o 45yo male with abd pain, diarrhea, fever, arthralgia. PE: low grade fever, tender abdomen.
           No evidence for obstruction. He has Crohn’s. Arthritis will:
           Will improve with tx of Crohn’s disease
o AS:
         Improves with activity
o   On PE, pts with AS will have
         Increased thoracic kyphosis
o   Most common extra-articular finding in AS:
         Anterior uveitis
o   Reactive arthritis reaction to:
         Intestinal or GU infection
o   Enteropathic arthritis
         Correlates with severity of IBD
o   First line tx of psor arth
         NSAID
o   In reactive arth, antibiotics are used
         Usually just for urethral infections
o   In addition to arth and urethritis, another another feature common to reactive arth is
         Conjunctivitis
o   Common cause of enteropathic arth:
         Crohn’s disease (microbes cause reactive arthritis)
o   Psoriatic arth complicated by
         Nail changes and finger joint deformity

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