musculoskeletal pathology

Handout ndash REVIEW SISTEM GERAKOleh dr Zainuri Sabta Nugraha

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MUSCULOSKELETAL PATHOLOGY

- Fracture ndash hematoma activation of osteoprogenitor cells BV proliferation procallus bony callus formation and mineralization organization of bony trabecular orienting along stress lines

- Osteomyelitis ndash Can have abscess necrotic bone (sequestrum) or new bone growtharound devitalized bone (involucrum) most commonly due to Staph aureus need Bx andculture to rule out cancer (ie Ewingrsquos sarcoma) can see bacterial colonies empty lacunae (dead osteocytes) and suppurative inflammation w PMN infiltrate

- Pagetrsquos Disease ndash probably due to paramyovirus lytic mixed and sclerotic phases overlap mosaic pattern in lamellar bone which is thickened uarrvascularity thickening of trabecular bone irregular tortoise shell patterns of bone deposition (lamellae in multipledirections) pt more prone to fracture and uarrrisk of osteogenic sarcoma

- Osteosarcoma ndash malignant cells making bone matrx most common primary malignant tumor (besides MM and lymphoma) bimodal age distribution (fist peek in teens) common occurs around the knee (lots of bone mass) often high-grade and requiring adjunctive chemo (chondromsarcoma is just surgical Tx) can be due to Rb mutation MDM2 overexpression benign tumors prosthesis chronic OM w draining sinus and radiation all uarrrisk path requires gt90 tumor necrosis to say that chemo was effective

- Chondrosarcoma ndash neoplastic cartilage 2nd most common malignant matrix-producing bone tumor pt gt 40 YO and male glassy blue appearance can see calcification and necrosis uarrcellularity and multiple nuclei in lacunae

- Metatstatic disease in bone ndash most common skeletal malignancy via direct extension lymphatic vascular spread intraspinal seeding sources include prostate (multiple lytic lesions w sclerosis) breast kidney and lung neuroblastoma Wilmrsquos osteosarcoma Ewingrsquos and rhabdomyosarcoma in kids presence of glandular cells = metastatic

- Multiple Myeloma ndash multifocal destructive bone lesions axial location (vertebrae ribs skull) punched-out defects w intense proliferation of plasma cells

- Rheumatoid arthritis ndash perivascular infiltrates uarrvascularity organizing fibrin deposition uarrPMNrsquos juxta-articular erosions subchondral cysts pannus ankylosis exaggeration of synovium w proliferation of lining cells intense lymphocytic infiltrate

- Degenerative joint disease ndash fibrillation of articular surface uarrgranularity eburnation (ivory-like polishing of bone ends bone-bone contact wo intervening cartilage) joint mice (pieces of cartilage in joint space) osteophytes loss of articular cartilage can see clefts

- Gout ndash acute arthritis or chronic tophaceous gout histiocytes and giant cells trying to surround and wall off crystals- Fibroblast fibroma fibrosarcoma- Adipocyte lipoma liposarcoma- Smooth muscle leimyoma leiomyosarcoma- Skeletal muscle rhabdomyoma rhabdomyosarcoma- Endothelium hemangioma angiosarcoma- Nerve sheath cell neurofibroma schwannoma MPNST- Sarcomas grow quickly expand and compress surrounding tissue pseudocapsule true capsule exists in benign lesions sarcomas spread hematogenously to lung liver and bone whereas carcinomas spread via lymphatics uarrsarcoma risk w radiationgenetics environmental factors lymphedema- Grading ndash based on pleiomorphism cellularity mitotic activity necrosis vascular nerve invasion intermediate grade treated the same as high-grade (w adjunctive chemo)

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Nodular Fasciitis ndash volar aspect of forearm solitary rapidly-growing mass that mayregress can see fibroblasts mesenchymal mucin inflammatory cells and extravasatedRBCrsquos can be confused w sarcoma (high cellular w mitotic figures) reactive condition- Malignant Fibrous Histiocytoma ndash large unencapsulate mass in retroperitoneum orextremity tumor is hemorrhagic and necrotic storiform-pleiomorphic pattern(multinucleated cells swirling growth pattern)- Lipoma ndash most common soft tissue tumor in adults often ASx encapsulated normal fat- Liposarcoma ndash not due to malignant transformation of lipoma found in extremities andretroperitonuem myxoid is most common type will see myxoid stroma fine branchingvascular network and lipoblasts in various stages of differentiation

MUSCULOSKELETAL IMAGING

Arthritis

- ABCrsquos of Arthritis ndash Alignment Bone Cartilage Soft Tissue- Bone ndash inflammatory arthritis periarticular generalized osteopenia OA preserves bone

mineralization assess mineralization in mid-shaft of metacarpal bones

- Cartilage ndash inflammatory arthritis causes early erosions in bare areas of bone within joint not covered by articular cartilage width of joint space indirect measure of articular cartilage narrowing in almost all arthritis

- OA ndash joint space narrowing sclerosis protrusions of osteophytes but no erosions DIP PIP 1st CMC ulnar drift normal mineralization can have subcondral cysts

- RA ndash MCP PIP caparl joints distal radial-ulnar joint marginal erosions in bare areas uniform joint space narrowing (entire joint inflamed) no osteophytes (inflammation prevents bone growth) symmetrical involvement periarticular diffuse osteopenia

- periarticular swelling subluxations - PA ndash joint space irregular erosions covering entire joint effusion widens joint space

- Soft Tissues ndash Reiterrsquos produces swelling of entire digit (sausage digit) generalized soft tissue sweeling in PA and Reiterrsquos focal swelling in RA and gout (tophi ndash lumpy-bumpy soft tissue swelling cut out sharply-circumscribed erosions away from the joint)

- PA ndash classic = symmetrical involvement of DIP common = pauciarticular distribution of- erosive changes less symmetrical vs RA several joints involved in one digit (sausage digit)

marginal erosions fluffy periostitis near involved joint (new bone growth) fusiform soft tissue swelling fusion across severely affected joints normal mineralization

- Reiterrsquos ndash similar to PA but involves feet and SI joints (bilateral but not symmetrical) pauciarticular w several joints involved fluffy periostitis (spicules coming off margin)

- AS ndash symmetrical SI joint inflammation erosions fusion also affects hips knees spinal erosions syndesmophytes (bridging osteophytes) fusion (Bamboo spine) fluffy periostitis spine pseudoarthrosies (fracture through fused spine pain and

- neurological deficits)

- Gout ndash cystal-induced arthropathy involves great toe MTP asymmetric involvement in other joints bizarre non-marginal erosions and tophi asymmetrical lumps and bumps normal bone mineralization late bony changes erosions are sharply circumscribed w

- overhanging edges

Tumors

- Aggressive ndash poorly defined margins periosteal reaction (ie Ewingrsquos sarcoma ldquohair-onendrdquo appearance fine lines coming off bone indicating aggressive growth) no marginsseen w permeative pattern (most aggressive)

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- Nonaggressive ndash well defined margins (ie NOF) absent or mature periosteal (arrested thickening of bone) reaction

- Bone matrix ndash solid cloud-like or ivory (most dense) due to calcification of osteoid

- Carilage matrix ndash stippled flocculent or rings-and-arcs cartilage ossifies around periphery looks like small balls

- Osteosarcoma ndash MRI to assess intra and extraosseous extent of disease uarrdensity inside and outside of bone calcified soft tissue mass need MRI to assess bone involvement for limb-sparing surgery

- Chrondrosarcoma ndash involves pelvis femur tibia shoulder found in older pt can see irregular calcifications typical of cartilage matrix

- Ewingrsquos Sarcoma ndash highly aggressive ill-defined margins permeates bone hair-on-end sunburst reaction due to pushing out into soft tissue and periosteum canrsquot contain reaction soft tissue extension MRI better shows margins

- Simple Bone Cyst ndash common in children proximal humerus expansile w sharp margins no bony matrix or periosteal reaction fluid filled mass pushing outward ASx until fracture (malignant lesions usually painful) fallen fragments in cyst for Dx may need surgery

- Fibrous dysplasia ndash unknown cause mono or polyostotic grey homogenous matrix (ground glass) frequently expansile involve proximal femur pelvis

- Pagetrsquos Disease ndash paramyxovirus common in elderly usually ASx can produce fractures or degenerate into sarcoma thickened trabeculae and uarrwidth of bone uncontrolled local bone metabolism

- Osteoid Osteoma ndash small benign bone-forming lesion adjacent intense sclerotic bone formation despite small size of lesion seen in kids young adult males can be painful (use ASA NSAIDs) may resolve over time or use CT-guided RF ablation

Trauma

- C-Spine ndash lateral AP odontoid LR oblique views lateral view allows visualization of prevertebral soft tissues (swelling suggests bone injury) assess alignment w anterior spinal line (not reliable in elderly w osteophytes) posterior spinal line (most important)

- spinolaminar line (junction of lamina at base of spinous process)- Hangmanrsquos Fx ndash usually hyperextension w massive prevertebral soft tissue swelling - Jefferson Fx ndash break in C1 ring due to axial load pushing C2 up and displacing fragments laterally

seen in young males in diving accidents- Odontoid Fx ndash hard to find non-displaced due to hyperextension or mixed mechanism- Anterior shoulder dislocation ndash goes down and medial after relocation can see impaction fracture

on lateral humeral head (Hill-Sachs deformity suggests prior dislocation) - Acetabular fracture ndash seen in MVA femoral head in superior-lateral position can see intra-articular

fragment of bone in acetabulum (remove or get early arthritis) sitting position knee driven posteriorly pushing femoral head out posteriorly

- Radial head fracture ndash subtle use fat-pad sign (joint effusion good sign of occult fracture fat pad displaced due to hemarthrosis seen in falls w outstretched arms and elbow pain can be non-displaced take another x-ray 7-10 days later to better see fracture

- Child abuse ndash corner fracture (periosteum ripping away bone fragment bleeding cloaking thickens and calcifies w repetitive trauma can be exuberant and mimic bone forming tumor) posterior rib fracture multiple fractures of different ages subdural hematoma and SAH due to shaken baby

- Knee ndash best seen w MRI ndash PCL ACL lateral medial meniscus

Infection Metabolic and Systemic Bone Diseases

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- OM (osteomyelitis) ndash acute presents w subperiosteal abscess + elevation of periosteum early destruction of femoral cortex immature periosteal reaction mimics tumor chronic OM ndash walled-off area w persistent infection low grade inflammation can track along the bone soft tissue sinuses dense sclerotic reaction cloacae (tracks in bone)

- Vertebral disc space infection ndash starts in vertebral endplate spreads to involve disc destruction of disc narrowing of disc space

- Renal Osteodystrophy ndash hyperPTH bone resoprtion at many sites inducing osteoporosis and osteosclerosis renal rickets in kids see subperiosteal resorption w fuzzy bone margins (see in margins of middle phalanges)

- Osteonecrosis ndash bone infarction and death common in femoral head best seen w MRI- Sickle Cell Disease ndash can result in osteonecrosis due to stasis of blood infarcts in femoral head

h-shaped deformities due to central compression of vertebral bodies- Leukemia ndash lytic lesions periosteal reaction simulating infection- Neuroblastoma ndash mets to bone 1048774 widening of skull sutures

CARTILAGE PHYSIOLOGY AND OSTEOARTHRITIS

- Joint = capsule w synovial fluid inside (from synovial lining cells)- Capsule ndash variable thickness often ligamentous provides support- Synovial Lining ndash covers all areas within joint except cartilage highly vascular w lypmhatics and nerves contains hyaluronan lubricin and synovial lining cells- Synovial Lining Cells ndash monocyte-derived (Type A basis for immune activation and autoimmunity) fibroblast-derived (Type B) dendritic cells mast cells lining cells are source of nutrients for chondrocytes (on subchondral bone plate which is avascular)

- Muscles tendons have most of stress distribution neural input important (reflexes prepare joints for stress)

- Atypical osteoarthritis ndash due to neurological system that is not intact lack of fine position sense pt w DM peripheral neuropathy at risk aggressive arthritis especially in legs

- Synovial fluid ndash primary metabolic supply for cartilage not efficient cartilage matrix has slow turnover chondrocytes at bottom of cartilage plate inactive but respond w disease metabolic supply darr w age possibly leading to arthritis - Lubrication via hyaluronic acid (long sugar) component of joint fluid and cartilage

- Cartilage structure ndash 70 water ability to allow water to leave w compression and reabsorb water w relief of pressure = resiliency chondrocytes at bottom of cartilage generate matrix (lots of PGrsquos) collagen comes up in arcs from bone in triple helix (if dysfunctional or modified collagen can lead to osteoarthritis)

- Type II collagen most common in cartilage Aggregan is the primary PG- PG (proteoglikan) ndash protein core filament GAGrsquos stuck as side chains (ie heparin keratan

both are sulfated which attract water chondroitin also a side chain) pressure forces water off sulfate groups water reattaches wo pressure PGrsquos attached non-covalently to HA stabilized by link proteins (all components made by chondrocytes)

- PGrsquos found in other CT types comprise 20 of cartilage volume- Chondrocytes gets nutrients from synovial fluid make HA all under metabolic control

(cytokines GFrsquos) constant production and metabolism- Matrix metabolism changes w age - darrchondroitan sulfate (darrwater retention) smaller PG

aggregates shorter HA darrnutrient supply cannot produce large amounts of matrix- MMP ndash degradation of CT structures controlled by TIMPs (slow cartilage degradation)- Scleroderma ndash too much CT accumulating- Injury ndash chondrocytes uarrmatrix production but not as much Type II collagen production

Osteoarthritis

- Imaging ndash interspace narrowing marginal osteophytes subchondral sclerosis (thickening of bone plate beneath cartilage) subchondral cysts misalignment

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- Affects cartilage in weight-bearing joints pain related to use worse during the day minimal morning inactivity stiffness (lt20 min) darrROM (crepitus on passive ROM) joint instability bony enlargement of joints (not inflammation which is spongy)

- Age is biggest factor (idiopathic) also female sex obesity (affects legs) hereditary factors trauma NM dysfunction (neuropathy disrupts joint mechanics accelerated OA) metabolic disorders

- OA features progressive cartilage loss subchondral thickening marginal osteophytes (uneven hypertrophied bone edges)

- Locations ndash knee hip lumbar cervical spine hands (DIP ndash Heberdenrsquos nodes PIP ndashBouchardrsquos nodes CMC ndash base of thumb most common in hand most functional effect) foot (MTP of first toe)

- Does NOT involve ndash ankle MCP (except in thumb) wrist elbow shoulder- Women ndash higher incidence DIP most common then knee and hip involvement- Hip ndash subchondral sclerosis loss of joint space pain radiating down medial leg (vs bursitis ndash

lateral leg pain)- Ankle OA suggests another process is also at work ndash ie DM neuropathy NM disease previous

trauma overuse predisposing metabolic disease (CPPD ndash pseudogout)- OA secondary to DM neuropathy ndash MTP 2-5 also involved midfoot usually spared- Underlying disease associated w OA and CPPD ndash hemochromatosis hyperPTH hypothyroidism

hypoPO4 hypoMg neuropathic joints trauma aging hereditary- Management ndash progressive exercise to uarrfunction endurance strength (darrfalling risk)- Strengthening exercise ndash low-impact continuous (15-30 min) 3xweek creates better joint

alignment and slows OA progression- Acetominophen ndash first line therapy pain relief comparable to NSAID w less toxicity- NSAID - darrinflammation SE include GI renal worsening CHF edema use generic and low-dose

first neither NSAIDs nor Tylenol affect disease progression- COX2 Inhibitors ndash pain relief equivalent to older NSAIDs darrGI toxicity no effect on platelets but

can have renal toxicity and edema- Tramadol (codeine) ndash affects opioid and 5HT pathways can cause constipation or rash often

added to NSAID or acetaminophen regimens (combining small multiple doses of several meds can treat OA while avoiding SErsquos)

- Codeine Oxycodone (narcotic analgesics) ndash can induce tolerance bowel immotility avoided by adding Propoxyphene or Tylenol 3 (w codeine) in darrdoses to other regimens

- Topical anesthetic ndash Capsaicinndashcontaining drugs for Sx relief- Intra-articular Tx ndash steroids or HA (not as commonly used)- Other Tx ndash glucosamine (Sx benefit prevent darr in joint space) Tetracycline (darrMMP activity)- Surgery ndash arthroscopy (trim cartilage ligaments) total joint replacement- Summary ndash make sure pain is joint-related donrsquot avoid exercise weight loss as treatment 1st

line ndash Tylenol 2nd line ndash NSAID intra-articular agents lavage opioids 3rd line ndash arthroscopy osteotomy joint replacement

RHEUMATOID ARTHRITIS

- Morning stiffness gt1 hour (any inflammatory arthritis vs structural osteoarthritis)- Polyarthritis ndash at least three joint areas hands almost always involved symmetry typical- No imaging abnormalities early eventually get cartilage bone erosion in hand feet- Rhematoid nodules in 30 but specific Rheumatoid factor in 80 but not specific- Need to determine if there is inflammation when pt presents w joint pain look for warmth morning stiffness

erythema swelling also need to determine if joint is truly affected or if adjacent tissues structures are affected- Normal joint fluid lt200 WBC osteoarthritis 200-2000 gt2000 can be RA psoriatic arthritis gout SLE etc

septic arthritis can have WBC gt 100000- Chronic polyarthritis ndash can be RA juvenile chronic arthritis systemic rheumatic diseases (systemic vasculitis

has arthritis can be mistaken for RA until other organs involved) spondyloarthropathies (akylosing spondylitis Reiterrsquos Syndrome) and psoriatic arthritis

- RA involves wrists MCP PIP of hands (vs OA DIP PIP base of thumb)- RA can also involve large joints like knees shoulders elbows (OA can also affect knees)- RA also involves ankles feet hip cervical spine (LS spine in OA lower spine and sacral ileitis in

spondyloarthropathies) TMJ larynx- Psoriatic arthritis ndash affects hands w psoriatic skin rashes and nail abnormalities inflammation of DIP (sauage

digit in every finger)

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- Hands in RA ndash later can see pronounced interosseous muscle atrophy PIP swelling ulnar deviation of fingers (subluxation under metacarpal heads) along with radial deviation at the wrist

- Patients can have OA w RA ndash abnormalities in DIP as well as PIP and MCP- Lumpy swelling of tendon sheaths (tenosynovium lining tendons) very uncomfortable and limit hand function- Wrist swelling carpal tunnel syndrome (median nerve compression) atrophy of thenar muscles and

sensory losses (can become permanent) treat w splinting local steroid injections surgery- Swan neck deformity ndash hyperextension at PIP DIP passively pulled into flexion contracture not just due to

arthritis but also tendon slippage- Boutonniere deformity ndash PIP in flexion DIP in hyperextension- Mallet deformity ndash dt tendon slippage extensor tendons slip to volar side to all tendons work to flex the finger- Early in RA ndash bones are normal joint space normal little soft tissue swelling some osteopenia near the joint

only (local effect of cytokines like IL-1 TNF osteoclast promoting cytokines) which is precursor to true erosion- Later in disease - darrjoint space cartilage has been eroded gaps of erosion in bone cortex eventually no

cartilage space left large erosions synovial pannus eating into bone- Erosions occur on bone side first articular cartilage only present on weight-bearing surface of bone bare areas

of bone lack cartilage pannus can attach directly to bare areas wo having to go through cartilage first- Can also see tendon rupture due to tenosynovitis and rubbing against eroded bone

- RA vs OA in hands ndash RA has more prominent early soft tissue swelling periarticular demineralization (OA has reactive bone and sclerosis in response to darrcartilage) more erosions (rare in OA except for collapsed cysts) rare reactive bone formation more severe joint deformity both have joint narrowing (cartilage damaged in both directions)- RA ndash wrist MCP PIP OA ndash DIP PIP thumb base

- RA in feet ndash hard to examine swell under other conditions eventually get hallux valgus deformity (toes point outward) toe contracture (weight-bearing pad under MTP slips forward pt walking on metatarsal heads painful toe subluxation ulceration)

- Swelling deformity in ankles are seen along w Achilles and extensor tendon involvement also progressive flattening and eversion of foot requires surgery w complex fusion to restore anatomic position of foot

- Some erosion evident in MTP early on progresses so toes no longer associate w appropriate metatarsal- RA from early to late adulthood (30-60) more common in women- No evidence that infection present in RA joint possible to have immune mediated events that reflect infection

elsewhere- Reiterrsquos Syndrome and reactive arthritis ndash clear link between infection elsewhere (ie GI) and development of

arthritis- RA did not exist before contact between Old and New World (environmental factors)- uarrLymphocytes in RA synovial fluid also uarrmonocyte macs thickening of synovial lining cells and fibroblast

layer- B-cells are a small but significant proportion of synovial lining cells express CD5 associated w autoAB

production Rheumatoid factor and other autoABrsquos made in joint functions like LN in RA but RA can occur in pt w agammaglobulinemia (so autoABrsquos are not necessary for RA)

- Rheumatoid factor = AB against immunoglobulin (usually IgM) antigen for RF is Fc portion of IgG ABrsquos alone can create immune complexes but present in many other diseases (endocarditis chronic lung liver disease Sjogrenrsquos Syndrome) not all RF+ pt have RA

- uarrT lymphocytes and uarrAPCrsquos to activate T cells in joint fluid accumulation not random (some clones are dominant) associated w specific MHC alleles (T cell function important in RA pathogenesis T cell clones can transfer disease to another host)

- No identified antigen that uniformly elicits T cells response in RA Tx that remove T cells in joint not effective T cells quickly repopulate w more aggressive clones

- Metaplasia of joint lining into lymphoid organ immune cells joint lining cells and cartilage all together interactions between these and T cells dendritic cells macs fibroblasts eroding cartilage all contribute to disease

- Inflammatory leukocytes adhere to luminal side of epithelium cognate cell-cell interactions (specific receptor-ligand) or secreted cytokines acting locally

- TNF from synovial monocyte mac autocrine feedback to mac to make IL-1 IL-1 TNF activate synovial fibroblasts transformed to make cartilage-degrading proteases instead of joint lubricant also make inflammatory PGrsquos cytokines chemokines

- TNF acts on endothelium to uarradhesion molecules for leukocytes monocytes respond to ODF (osteoclast differentiating factor) and turn to osteoclasts (accelerated 100x w TNF and IL-1) which attack bone after fibroblast degradation of cartilage

- Cytokines T cell activation uarrTNF IL-1 in joint can enter systemic circulation constitutional Sx

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- Therapy targets ndash y-IFN (Th1 cytokine) IL-15 (T-cell GF) IL-17 (activates synovial fibroblasts) other mediators ndash PG arachadonic acid metabolites MMP NO darrpH in joint and at cartilage-pannus junction reactive O2 species other proteases

Ligamentous Strains

- Grade I ndash intact structurally no laxity microscopic disruption- Grade II ndash partial tear w laxity definite endpoint- Grade III ndash complete disruption wo endpoint (flail joint) requires surgical repair- Ligaments stabilize joints by allowing movement in only certain planes injury occurs when there is

motion in abnormal plane or excessive motion in normal plane need subluxation or dislocation to significantly injure ligament

- PE ndash joint swelling in proportion to degree of injury ecchymosis tenderness over ligamentous attachments restricted AROM and PROM

- Dx ndash x-rays for Grade II III or severe trauma stress radiographs for determining endpoint in ankles MRI for knee shoulder ankle (gold standard)

Principle of Rehabilitation

- Acute Phase - darrpain inflammation (PRICE ndash protection relative rest ice compression elevation) want to keep as active as possible unless bone is fractured can also use NSAID corticosteroid injections splinting bracing compression wraps surgery

- Avoid steroids in Achilles and patellar tendons (risk of rupture)- Recovery Phase ndashneed 60 ROM to enter this phase ROM can be restored passively or actively

need uarrmuscle strength (start w isometric isotonic isokinetic) closed chain exercises helpful and shouldnrsquot be painful uarrendurance w uarrreps darrresistance

- uarrproprioception w balance agility drills- Maintenance Phase ndash return to activity in progressive functional way start CV conditioning as

early as possible functional progression of activity (reestablish motor skills) prevent re-injury (correct underlying biomechanical factors education)

MUSCULOSKELETAL GROWTH AND DEVELOPMENT

Torsional Deformities of Lower Limbs

- Torsion ndash twisting in reference to tibia internal external- Version ndash twisting in reference to femur retroversion anteversion (outward proximally)- In-Toeing ndash common can originate at foot knee or hip- Metatarsus adductus ndash turning-in of foot in 0-18 months limited to forefoot spontaneously

resolves in 80 can treat w casting or rarely surgery- Internal tibial torsion ndash 6-18 months most spontaneously improve defined by transmalleolar axis

(movement of fibular with respect to medial aspect of distal tibia medial malleolus 1048774 if extreme fibula in front of medial malleolus)

- Femoral anteversion ndash 3-9 years usually normal growth pt has feet straight forward but knees inward not problematic even if it persists no arthritis or functional problems rotation of femoral head with respect to femoral condyles (ie femoral head rotated

- vertically away from plane of condyles)- In-toeing can also be cause by clubfoot (entire foot involved) atavistic first toe (overactive

abductor hallucis only) neurologic problems (cerebral palsy)- Out-toeing ndash less frequent than in-toeing- Calcaneovalgus foot ndash foot is excessively dorsiflexed to the leg and turned outward improves

spontaneously within a few weeks after birth packaging problem- External tibial torsion ndash uncommon red flag for CP or myelodysplasia knees pointed straight

ahead but feet turned outward- External rotary contractures of hip ndash 0-18 months improves spontaneously Angular Deformities of

Lower Limbs- Valgus ndash deviation angulation away from midline- Varus ndash deviation angulation towards midline

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- PE ndash need to see if there is laxity about knee joint also test motion of all lower limb joints localize angulation assess alignment

- Radiographic ndash XR of whole hip lower limb and foot on same film both AP and lateral to assess alignment

- Labs ndash rule out renal rickets get Ca PO4 Vit D and alk phos Levels- Bowlegs (Genu Varum) ndash inward angulation with respect to midline (angle made by femur and tibia

opens inward) can be physiologic caused by Blountrsquos Disease (growth plate abnormality ndash uneven growth of proximal tibial epiphysis more growth laterally) rickets or metaphyseal chondroplasia

- Physiologic Bowing ndash 15o normal in infants legs move to neutral position by 18-24 months x-rays are otherwise normal track w Salenius and Vankka chart children start bowlegged normal knock-knee normal

- Infantile Blountrsquos Disease ndash canrsquot make Dx until 2 years old occur in overweight kids and those who are early walkers pt tends to have internal tibial torsion x-ray show excessive beaking on medial side of proximal tibia depression of medial plateau Stage IV

- disease can result in fusion of bones- Rickets ndash widened growth plates on x-ray- Knock Knees (Genu Valgum) ndash outward angulation seen in ages 3-5 usually normal developmental

variation but can be caused by renal osteodystrophy metabolic bone disease bone dysplasia

Developmental Dysplasia of the Hip

- Not always seen at birth continuum of subtle findings 1048774 subluxation 1048774 dislocation- Mechanical factors often responsible ndash small space (common in firstborns) breech presentation

(legs adducted) left hip more involved (left leg adducted commonly in utero)- DDH often presents w torticollis (head tilting rotation) and metatarsus adductus (both

mechanical problems) DDH more common in females (estrogen effect)- Hip at Risk ndash Major (abnormal clinical exam breech first-born and female family Hx) and Minor

(limited hip abduction sacral dimple foot and postural deformities)- Newborn to 2 months ndash Ortolani and Barlow tests most reliable x-rays unreliable USN allows

visualization of cartilage but may be too sensitive- PE ndash should be part of every well-baby exam infant needs to be relaxed Orolani - stabilize pelvis

flex hip to 90o adduct past midline the abduct and lift towards socket (can catch hip dislocations or subluxations which then relocate) Barlow ndash flex hip to 90o gently push posteriorly to dislocate

- Tx (0-6 months) ndash reduce femoral head into acetabulum abduct hip w Pavlik harness free range but limited range of motion make sure harness isnrsquot too tight avascular necrosis of femoral head

Crystalline Arthropathies

- Crystals build up in joint space and cause inflammation gout and pseudogout are very treatable no sex bias

- Gout ndash monosodium urate crystals (from uric acid) most common crystalline disease rarely found in shoulder

- Pseudogout ndash calcium pyrophosphate crystals (CPPD)- Hydroxyapatite ndash Dx requires EM and alozerine red common in shoulder (ldquoMilwaukeerdquo)- Calcium Oxalate ndash seen in pts on dialysis- Dx categories ndash infections inflammation degeneratie traumatic neoplastic (rarest)- ASx Hyperuricemia ndash allopurinol used to darruric acid production but many SErsquos donrsquot need to use

for every pt w uarruric acid (only ~15 actually have gout)- Gout can present as acute gouty arthritis or chronic tophaceous gout associated w obesity DM

hyperlipidemia HTN atherosclerosis EtOH acute illness (mono)pregnancy post-op negative associations ndash SLE RA amyloid dialysis

- Gout can co-exist w OA CPPD septic arthritis and others Renal Disease with Gout- Urate nephropathy ndash pt w hyperuricemia can get kidney damage but only if uric acid- consistently lt13 (most pt w gout are at 8-9) pt w uarruarruric acid should get allopurinol - Acute uric

acid nephropathy ndash crystalline arthropathies can lead to simultaneous bilateral microscopic obstruction of kidneys from excess uric acid crystals no stones

- evident on USN or CT no hydronephrosis evident for several weeks more common in pt undergoing induction chemo for leukemia lymphoma (get allopurinol w chemo)

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- Calculi ndash 90 of pt w kidney stones have calcium stones rare to find uric acid stones but many calcium stones form around a small uric acid crystal darruric acid helps to prevent calcium stones in pts w recurrent stones

Acute Gouty Arthritis

- Abrupt onset often at night usually monoarticular- Deep stabbing hot pain in a red warm swollen and extremely tender joint- Resolves in 3-10 days even wo Tx most pt have MTP involvement of big toe- Dx ndash urate crystals found inside WBCrsquos in the affected joint most pt have hyperuricemia but 15

have normal uric acid during gout attack (but hyperuricemia for many years before attack) x-ray has punched-out lesions w overhanging edges (uarrbone growth)

Causes of Hyperuricemia

- Decreased Excretion (90) ndash Dehydration starvation ketosis (post-up pt are NPO tissue trauma during surgery releases purines uarruric acid w purine salvage pathways) renal abnormality (tubular disorders) drugs (diuretics low-dose ASA) toxins (EtOH Pb) hypothyroidism

- Increased Production (10) ndash EtOH (2 beers can trigger gout attack) HGPRT deficiencyG6PD deficiency superactive PRPP synthetase myeloproliferative disorders (lymphoma leukemia mono) psoriasis

- Complete HGPRT Deficiency ndash Lesch-Nyhan Syndrome 1048774 uric acid overproduction mental retardation microcephaly compulsive self-mutilation gouty renal disease uric acid crystals present in urine but NOT gouty arthritis

- Partial HGPRT Deficiency ndash 1 of normal enzyme activity can avoid mental retardation (but still abnormal basal ganglia) early onset and severe arthritis gout renal disease

Acute Gout

- Crystals in WBC intense inflammatory reaction (crystals themselves arenrsquot harmful but host response is excessive WBCrsquos canrsquot destroy crystals engulf and release inflammatory mediators 1048774 severe inflammatory arthritis) crystals alone in a joint canrsquot

- cause gout- Unexplained features ndash initiation of attack self-limited nature of attacks joint distribution (big

toe most common but also other toes midfoot heel ankle knee rarely affects fingers but can coexist in OA Heberdenrsquos nodes in DIP rarely affects other joints) minor trauma or uarractivity can trigger episode

- Dx ndash clinical findings joint fluid aspirate under polarized light positive response to gout therapies classic radiographs

- Diagnostic arthrocentesis ndash aspirate joint fluid view using multiple polarizing lenses gout has needle-shaped uric acid crystals inside WBC that appear yellow pseudogout has rhomboid crystals that are blue

- DDx of 1st MTP toe inflammation ndash gout pseudogout RA OA traumatic arthritis sickle cell anemia OM bony infarct

- Complications ndash quality of life issues 1048774 pain darrmobility

Treatment

o First choice ndash indomethacin 35-30 mg qid tapering over five dayso Colchicine 06 mg one tablet hr max 12 tablets in first day then max 06 mg TID over the next week (most pt get significant SE after 8th pill) IV colchicines are dangerous but used as one-time dose post-opo Butazolidin ndash rarely used can cause irreversible aplastic anemia on first doseo Intra Articular steroids NSAIDs ndash donrsquot work well unless given very early in an attacko Narcotics ndash usually ineffective for pain relief- Prophylaxis ndash indomethacin 25 mg qd-bid colchicine 06 mg bid- Long-term anti-hyperuricemic treatment

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o uarrFrequency of gout attacks during establishment of long-term control need to use prophylactic doses to try to darrattacks during long-term therapy inductiono Allopurinol 300 mg PO qd to darruric acid productiono Sulfinpyrazone 100 mg titrated or probenecid 500 mg qd-bid ndash uricosurics (uarruric acid excretion use only if gout is due to darrexcretion donrsquot use drugs if excretion lt900 mg 24 hours or kidney stones will form)- 90 will have another attack within 5 years of first attack often have 5-6 attack the following year pt w lots of attacks or tophi (large uric acid conglomerates) should get long-term therapy to protect kidneys will often require 2-5 years of allopurinol to getresolution of severe tophi- Colchicine ndash from a plant difficult dosing SE ndash NVD skin reactions myelosuppression muscle disease neuropathy apalstic anemia thrombocytopenia- Indications for allopurinol ndash tophi uricosurics CIrsquoed (renal insufficiency w creatinine clearance lt80 urine uric acid gt 13 uric acid overexcretion) renal stones (any type) chemotherapy induction- Allopurinol DDIrsquos ndash azathioprine (competitive inhibitor of enzyme affected by allopurinol) cyclosporine mecaptopurine- Diet - darrhigh purine foods (brain heart kidney liver)

ORTHOPEDIC SURGERY

- Hip = ball and socket MCP TMP = hinge AC SC = fibrous sub-talar = saddle within joints are facets auxiliary joints discs menisci knee is complex joint w changing rotational axis

- Long bones ndash diaphysis (cortical bone highly vascular) metaphysic (trabecular area highly vascular) physis (growth plate in children) epiphysis (variable vascularity) cartilage at articular surface avascular (poor response to injury)

- Open (ldquocompoundrdquo) fracture = hole in skin grade 1 (lt1cm hole clean) grade 2 (1-10 cm) grade 3 (gt10 cm dirty)

- Simple fractures ndash oblique (most common) or transverse (straight across bone rare unless bone already weakened ie pathological fracture)

Comminuted fracture has multiple pieces butterfly fragment is fracture element w threepoint bend (+- twist) buckle fracture in children since bones soft enough to allow crushing instead of breaking Greenstick fracture in children since bones pliable enough to allow partial breakage stuck in bent position (requires complete refracture to set bone) Salter fracture = physeal fracture heal easily if aligned properly

- Angulation ndash described by where apex of fracture is pointing- Open fracture is surgical emergency risk for chronic OM the closer a bone is to the center of

body the more urgently it needs repair radial head fracture can be treated w sling but femur displaced scaphoid fractures and polytrauma require surgery

- Dislocation ndash components of joint have come apart no longer in contact w articular surface described with respect to direction of distal part of joint

- Most shoulder dislocations are anterior occurring during external rotation seizure can cause posterior dislocation (stronger back muscles)

- Subluxation ndash joint has come apart but components still intact less common- Ortho emergencies ndash open fractures some dislocations septic joints fractures that attenuate

skin or neurovascular structures- Septic joints can be post-trauma or dental procedure w prosthetic joint more common in

children (rich vascular supply capsule extends around metaphysic) if untreated can lead to joint degeneration should wash out joint if pus suspected (insidious onset of warm red painful and swollen joint)

- Compartment syndrome ndash occurs after injury emergent muscles compartmentalized by fascia to uarrpower fascia is taut 1048774 bruising bleeding swelling can exceed potential space bone fascia not pliable uarrpressure BVrsquos and nerves compressed

- 6 Prsquos of compartment syndrome ndash pain out of proportion to injury pallor (darrperfusion too late) paresthesia below injury pulselessness (too late) pressure pain to passive stretch

- Tendonitis bursitis ndash inflammation of tendon peritendon insertion or overlying bursa commonly due to overuse treat w RICE (rest ice compression elevation)

- Sprains Strains ndash grade 1 (pain but still functional) grade 2 (darrfunction) grade 3 (no function) stress = force strain = response to force

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Neuropathies ndash sciatica (low back pain) pinched nerve (consider referred Sx ndash ie obturator nerve runs down medial compartment from hip knee hip injury can cause knee pain) carpal tunnel syndrome (most common mononeuropathy in upper extremity) all treated w RICE

- Spinal deformities ndash scoliosis kyphosis ankylosing spondylitis DISH- Pediatric issues ndash OM DDH club feet infections are common in children- Acute shoulder pain is atypical (probably traumatic AC separation broken clavicle) chronic

pain more common- Adhesive capsulitis ndash fibrosis of capsule shoulder pulled in can be post-surgery MI injury or

due to other coexisting diseases pt has insidious pain and stiffness passive ROM = active ROM (but decreased) Tx w therapy to stretch shoulder

- Shoulder arthritis ndash bone spurs inhibit movement painful chronic condition in elderly passive ROM gt active ROM but still movement painful

- Shoulder impingement ndash rotator cuff tendons pinched under acromion compression of bursa usually gradual onset w night pain (but not awakening) anterolateral pain radiating down the arm painful arc impinged tendon weakens humeral head drops impingement worsens Tx w strengthening of rotator cuff anti-inflammatory meds rest

- Rotator cuff tear ndash limits voluntary motion of shoulder PROM gtgt AROM pt does well w arthroscopic surgery (rotator cuff = suprainfraspinatus teres minor subscapularis)

- Biceps tendonitis ndash distal rupture (lump closer to shoulder can reattach tendon to radial tuberosity restores supination) proximal rupture (lump closer to elbow) lateral

METABOLIC BONE DISEASE

- ECM of bone = osteoid (cross-linked Type I collage) and mineral crystals laid down over osteoid by osteoblasts

- Cortical laminar bone is thick on outside of most long bones resistant to fracture trabecular bone is loosely connected mesh less structurally resistant prone to fracture w darrCa or osteoid

- OB ndash from CT progenitors produce ECM proteins (collagen I and osteocalcin) produces AP (needed for mineralization used as serum marker for OB activity) regulated by TGF- β and IGF-1 left behind in bone as osteocytes to maintain function

- OC ndash multi-nucleated giant cells from hematopoietic precursors mediate bone resorption sealed contact area w bone 1048774 acidic environment lysosomal enzymes stimulated by IL-1 IL-6 TNF-α migrate into bone before beginning resorption

- Ongoing bone remodeling ndash OC breakdown for 7-10 days 1048774 OB bone reformation for 3 months complete turnover of bone every few years incomplete process once over 20-30 (bone resorbed gt bone replaced)

- Mechanical loading is stimulus for bone formation immobilization (bed rest) uarrresorption and darrformation seen in astronauts

- Osteoporosis- 15-25 of women will sustain OP fracture at some point 10 of men - OP = darrbone

mass remaining bone normal max bone density in mid-20rsquos steady loss of bone after five-year period of accelerated loss in post-menopausal women wo HRT but

- resume normal rate of loss afterwards- Fracture threshold = certain amount of bone to maintain integrity everyone falls

below threshold if they live long enough- Risk factors ndash polymorphism in Vit D receptor +family Hx thin body (obesity

uarrmechanical loading of bones) fair skin smoking white asian (black females have same risk as white men) GC excess from steroid therapy or Cushingrsquos

- Early OP is ASx unless there is fracture can occur w minimal trauma vertebral compressions most common along w hip and wrist fractures (uarrtrabecular bone) death rate from hip fracture is 10 (PE infection etc)

- End-stage disease ndash marked dorsal kyphosis loss of lumbar lordosis can cause arthritis erve compression chronic muscle pain

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- Dx ndash bone density more than 25 SD below mean for healthy young individuals poorly assess w x-ray need bone densitometry (DEXA) which measure bone thickness density given as gcm2 reported as T-score (ie -40 worse than -30)

- Bone markers ndash OB releases AP and osteocalcin (less available but more sensitive) OBrsquos active in OP but canrsquot keep up w resorption OC markers are pyridinoline crosslinks and N-telopeptide (part of Type I collagen after degradation) markers useful for following

- response to Tx- Osteopenia ndash caused by hypogonadism (both men women seen in post-menopause

wo HRT most pt w OP are hypgonadal) hyperPTH and hyperTH uarrOC activity Cushingrsquos darrOB activity osteomalacia cancer (multiple myeloma)

- Prevention ndash adequate Ca intake women need supplemental Ca pre-menopause (1 gday) young women should get 500 mgday (ie one Tums) avoid hypogonadism in younger pt high risk w hypothalamic amenorrhea (hyperPRL or exercise-induced)

- weight-bearing exercise- Tx ndash most important is to prevent falls- Calcium Vitamin D ndash RDA for Vitamin D is 400 units day should give 800 units- Gonadal steroid replacement - darrOC activity effective Tx and prevention estrogen

probably as effective as bisphosphonates long-term estrogen uarrbone mass and darrfracture risk replace hormones in men w testosterone deficiency and deficient pre-menopausal

- women- Raloxifene ndash SERM uarrbone density darrfracture risk no trophic effect on breast

uterus uarrhot flashes not as potent as estrogen but still uarrblood stasis (thrombosis)- Bisphosphonates ndash aledronate risedronate potent inhibitors of OC sustained uarr in

bone density darrfracture risk by 50 possible erosive esophagitis w bleeding need to take w full glass of water no food or supine position for 30 minutes (now available as one pill week)

- Calcitonin - darrOC activity slows bone loss but doesnrsquot restore bone (unlike bisphosphonates) available as nasal spray or injection can provide pain control for acute fracture SE include NV flushing used as 3rd or 4th line agent

- Any pt on GC for gt1 week will have OP pt should have adequate Ca VitD bisphosphonates can reverse slow GC-induced OP start concurrently Osteomalacia Rickets

- Case ndash resection of 15 feet of SI due to Crohnrsquos Ca low normal darrPO4 albumin Hb carotene cholesterol (malabsorption) uarrAP zero VitD uarrosteoid seams (unmineralized osteoid)

- Osteomalacia can be due to malabsorption fat soluble vitamins often first manifestation

- Generalized bone pain in absence of fractions (never seen in OP)- Rickets in children causes bone deformities osteomalacia is inadequate bone

mineralization in adults- Most commonly due to VitD deficiency (inadequate intake sunlight) or resistance

leads to PO4 deficiency can also be caused by malabsorption renal failure severe liver disease hereditary syndrome

- Second major cause is PO4 deficiency secondary to renal tubular disease tumors XLR hypoPO4 or PO4 binders Al and F also inhibit bone mineralization in high amounts

- Bone disease caused by darrPO4 not darrCa darrVitD darrCa absorption from GI secondary hyperPTH serum Ca normalized at the cost of increased bone resorption phosphaturia (renal Ca absorption and PO4 excretion) and hypoPO4 inadequate

- bone mineralization osteopenia if severe PTH not adequate darrserum Ca- Patient presents w bone pain and pathologic fractures darrbone density hypoPO4

uarrAP from compensatory OB activity uarrPTH possible late darrCa

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- Pseudofracture ndash fractures only go halfway through bone thought to be widening of space around nutrient arteries

- Children ndash bowing of legs w weight-bearing deformation also get rachitic rosary (uarrcostochondral joint junction w bulging) children also short

- Tx ndash treat underlying disorder give Vitamin D if deficient give active form w renal dz Pagetrsquos Disease

- uarrBone turnover possibly due to viral infection uarrbone resorption exuberant compensatory increase on bone formation thick abnormal bones w uarrbone density

- Most pt ASx possible Sx include bone pain deformity if severe can have marked deformation of arms and legs prone to fractures arthritis nerve compression uarrrisk of osteogenic sarcoma

- Dx - uarrAP and characteristic radiologic appearance bone scan determines extent of disease then x-ray involved areas

- Tx only if symptomatic w pain deformity arthritis nerve compression bisphosphoates more potent than calcitonin

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ORTHOPEDIC SURGERY

















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musculoskeletal pathology

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