Musculoskeletal

THOROUGH assessment of the patient--don't be distracted by the fracture!  Could be internal trauma that's much more emergent!

• head: mentation changes, sz, anisocoria, epistaxis, otorrhea
• spine: non-ambulatory, pain perception in all limbs?, Neuro deficits in CP, reflexes?
• Thorax: pulmonary contusions,pneumothorax,rib fractures, diaphragmatic hernias, hemothorax, traumatic myocarditis
• Abdomen: uroabdomen, traumatic hernia, GI perforation, hemoab
• other limb:

• Closed: no external wound, fracture does not communicate with outside environment.  Most common
• Open: Fx communicates with outside environment. Bone penetrated skin from within vs object through skin breaks bone

• bone penetrates skin from within (may not communicate with wound on exam).  
• Wound <1cm, minimal soft tissue damage
• low energy trauma
• often simple fracture
• minimal contamination
• often treated like a closed fracture

• external force creates wound
• >1cm
• moderate soft tissue damage
• high energy trauma
• oftin comminuted
• may or may not treat likely a closed fracture

• Substantial soft tissue damage
• high energy trauma
• often shearing injuries and/or severe comminution
• requires careful planning.  
• 3 subtypes. 
• IIIa: no major reconstruction required
• IIIb: can't be closed without reconstruction
• IIIc: major arterial injury

• Amputation or near amputation.
• Severe soft tissue, neurovascular damage
• usually treated with amputation

• Closed: external computation (bandage, splint) to prevent worsening, becoming open, increase comfort. Analgesics, await definitive fixation
• Open: control hemorrhage, sterile bandage, check neuro/vascular, culture, abx, analgesics, TEMP bandage and wound care before definitive fixation.

• Evaluate each joint for: 
• crepitus
• ROM
• effusion
• pain
• instability

• Check for cruciate disease/stifle instability
• Patella/fibella 
• tibial tuberosity/head of fibula
• Drawer in flexion but not extension, prop their foot off the floor (with yours) if necessary
• Only partial if you get cranial but not caudal

• Cup cranial distal femur with leg at standing angle, index finger from patellar down tendon onto tibial tuberosity,flex hock without flexing stifle
• diagnostic for complete CCL tear

Animal in lateral, push against hip and rotate leg to open hip.  Hip will “clunk” back down into acetabulum.  Indicates hip dysplasia

• Axial load (compression/tension): straight up and down force
• Bending: side to side force
• Rotation: twisting around axis

• Elastic deformation: stress vs strain where implant snaps back to original shape like a spring. No permanent. Straight line on graph
• yield point: where implant can no longer snap back to original shape but stays deformed, between elastic and plastic. 
• plastic deformation: post yield-point.  Where implant remains deformed after stress, curved slope on graph
• failure point:  Where implant will just break.  
• Ultimate strength: maximum stress before failure

• Pro: lots o f cheap pieces, for open fractures and infected wounds (plate would get infected), angular limb deformity or length discrepancy (fine control), can preserve blood supply better than surgery, maybe faster healing
• cons: scary, hard to radiograph, owner care at home, gets infected, still requires surgical suite and aseptic.

• classified by location of connecting bars.
• 1a: unilateral, only goes in one side and one angle
• 1b: unilateral biplanar, one side but multiple angles
• II: bilateral (uniplanar),one angle goes all the way through. 
• III: bilateral biplanar, through-and-through, multiple angles and sides. 
• successively stronger and stiffer
• Unilaterals for simple fractures and small animals
• bilateral for complex and/or large dogs

• Positive threaded: threads laid on top of shaft so WIDER at threads, more common
• negative threaded: threads cut into shaft, narrower at thread level. Weak points, don’t use!
• half-pins/end-threaded: penetrates both bone cortices but only one skin surface
• full-pins/center-threaded: penetrates both cortices and both skin surfaces.

• 3-4 pins/segment
• always use threaded
• 3x in diameter or 1/2 bone diameter from fracture (at least)
• place both farthest pins (prox and distal) in metaphysics then both nearest pins.
• rings must be at least 1cm from skin

• shorter is better (stiffer).
• Larger is stronger/stiffer, but leaves a bigger hole, so weaker in torsion/bending
• NO LARGER THAN 20-30% BONE DIAMETER
• pin-bone interface determines if it will loosen.

• Acrylic, polymethylmethacrylate - like a ribbon, you can mold however you want.  
• Used a lot in birds

• Prevents iatrogenic neuro and vascular damage when putting pins through soft tissues.  
• Otherwise, could cause neuropraxia, bleeding, limited ROM, etc.

• Prevent swelling!  Wrap entire leg at first to stop distal swelling. Then bandage fixator. (Can’t do humerus/femur)
• check clamps weekly
• triple ab ointment around pins, Tefla over incision, “fluff and stuff” around all tracts etc. 
• Bumper bandage once swelling has gone down to prevent external hardwar from injuring animal or furniture

• Most common complication of external fixator (16-100%)
• relies on good pin-bone interface
• caused by excessive micromotion, thermal/mechanical damage at time of application/insertion, or fatigue failure of cortex.

• very common
• acute (pin tract establishing itself)
• chronic (pin tract infections)
• C/S, abx

common in cats!

• pain-free, functional joint due to bone union
• remove articular cartilage, add fresh autogenous cancellous bone graft, rigid fixation at a funcitonal angle.

• cranial-dorsal, usually
• common in dogs, rare in cats
• dx via rads - Ilium, ischium and trochanter should be in triangle, not line
• hip dysplasia may be predisposing cause
• tx 1: closed reduction, ehmer sling
• tx 2: open reduction and sx stabilization. Many choices, none are good
• tx 3: salvage procedure - FHO, total hip

• hip: sling
• elbow: cast/splint

• LATERAL luxation more common
• reduced in flexion and stabilized in extension
• full cast or splint for 10-20d

• medial shearing injury most common
• tx open wound first!  Missing parts = unstable (collaterals)
• Tx 1: ligament reconstruction, try this first (surgical grade fishing line)
• tx 2: arthrodesis. If tibiotarsal not involved, can do a partial. SALVAGE procedure. 
• MOST MOVEMENT OCCURS IN TIBIO-TARSAL JOINT

• most mvmt at radiocarpal joint
• most support is palmar fibrocartilage - does not regenerate
• Conservative tx not successful.  Usu pancarpal arthrodesis

• Osteogenesis: cells - osteoblasts that survive transfer
• Osteoconduction: matrix - graft is a scaffold
• Osteoinduction: factors - graft induces cells to make new bone (BMP)

• can be due to physeal fracture (SH type 5 in distal ulna) or congenital
• angular limb deformity, shortened limbs, secondary malarticulation (elbow)
• catch early! or will have to do crazy limb lengthening procedures.

• gastrocnemius
• superficial digital flexor
• common tendon of the biceps femoris, gracilis, semitendinosis

• causes tarsal hyperflexion, swelling/nodule, separation/discontinuity.  Can be bilateral.
• knuckling or down in hocks or both due to what is ruptured (SDF = hocks, LDE = digits).
• USE U/S hyperechoic (disorganized collagen)
• tx 1: rest and splint for partial tears
• surgery: primary tendon repair with POST-OP PROTECTION 
• maybe arthrodesis for salvage

• middle aged, large breed dogs with decreased weight bearing on forelimb, pain on shoulder flexion with elbow extension, due to chronic inflammation - wear or chronic microtrauma
• dx: rads - osteophytes and radio-opacity in intertubercular groove.  Use cranioprox-craniodistal "skyline" view. U/S to confirm.
• tx 1: exercise restriction (2-3mo) + NSAIDs (try this first)
• Tx 2: arthroscopic tendon transection/release, tenodesis (screw tendon into humerus - new attachment)

• middle aged, large-breed
• presentation: decreased weight bearing in forelimb, pain on shoulder flexion.  Mimics biceps tenosynovitis. Can be incidental
• rads: calcification around tendon. "skyline". 
• px: good to fair with surgical resection of calcification.

• working breeds
• characteristic lameness: abduction of humerus and distal limb with carpal flip, adduction of elbow, limited shoulder ROM. Dx vs gait
• etiology: trauma, progressive fibrosis
• tx: tentotomy (sx excision and release of fibrosis) - DON'T WAIT
• px: excellent with surgery

• young dogs with distal femoral fracture treated with splints
• signs; stifle and tarsal extension - long, straight back leg. 
• etiology: fibrotic adhesions between quad and distal femur
• tx: surgical release, myoplasties, arthrodesis, amputation
• px: poor
• PREVENT!!!

• signalment: GSD
• cause: unknown
• dx: goose-stepping gait (circumduting gait in hind limbs)

• uncommon but in d/b/e
• tendon slips off calceneous
• unknown cause, shelties and collies
• meds don't work
• surgery works great (tendon reduction and suture technique, splint)

• anatomical reduction
• rigid fixation
• maintenance of blood supply
• early mobilization

• open reduction and internal fixation
• Pro: versatility, anatomical reconstruction so bone can share load, rapid return to weight bearing, minimal post-op maintenance
• Cons: SOFT TISSUE INJURY, hard to do, can't fix after, expensive.
• complications: delayed healing, soft tissue, implant failure/migration, implant-associated neoplasia

• strength of material caries with direction of force applied.  Bone is strongest in compression and weakest in tension
• Bones like to be pressed down on, not pulled or twisted

• incomplete - intact periosteal sleeve
• tx with splint or cast, esp if internal splint (fibula or ulna intact)

rapid reduction of pain and return to function

• blood supply
• control of interfragmentary strain = change in fracture gap when load placed. Fibrous is high, bone is low.

• strength of material varies with the rate at which force is applied.  
• Fast application of energy takes more energy to break bone, so more comminuted, more soft tissue injury and more compromised blood supply

• protect ONLY against bending!!!
• So only good for simple transverse interdigitating diaphyseal fractures
• DON'T USE THREADED
• usu require removal and anatomic reconstruction (soft tissue injury)

• it takes adults 2-3x as long to heal. 
• 2-3wks in littles for well-reduced. 
• proximal heal faster than distal

• clinical union: can remove external support or external fixator and begin more aggressive rehab.  Must be stable and able to support body weight unaided. Much earlier than radiographic union (bridging callus on at least 2 orthogonal views)
• Radiographic union: fracture line or gap no longer apparent.  Much longer.

implant failure and fracture healing

• anatomical is perfect reduction. Can load-share but lots of soft tissue damage
• biological is USEABLE reduction. Can be better because doesn't destroy blood supply

• almost never alone except in mandibular symphysis separations
• have to totally reconstruct the cylinder of the bone (anatomical) for it to really work - long oblique or spiral fractures, and tension band wiring to convert tensile forces to compressive.
• closed via twist or loop.

• prevents tibia from moving cranially or rotating internally, limits stifle hyperextension
• we don't really get why.
• dx: offloading, subtle lameness, sit test (sit over on one hip with leg bent or straight). Pain, thickening, fibrosis, effusion around stifle, muscle atrophy, asymmetry.
• +/- tibial thrust or cranial drawer. 
• rads: "fat pad sign" where fat pad squished from effusion, osteophytosis in chronic cases.  CT/MR/US not sensitive enough.

• secondary to instability from complete CrCL rupture
• PAIN!  Worse lameness. Click? 
• medial meniscus, caudal portion.  "bucket handle". 
• REMOVE - it hurts!

• Conservative management: LIMITED population. Small dogs (<15kg) do okay but it takes months. Rest, NSAIDs, braces. Sx with meniscus
• intracapsular repair: graft put in joint to replicate CrCL. Hard to do. Grafts break eventually. 
• ExtraCapsular repair: easy, cheaper. suture may fail. Fabella to patellar tendon or bone anchors.
• Tibial Osteotomy (TPLO, TTA, TWO, cTTA, CBLO, TPLWOW...): move tibial crest cranially to change angle so femur doesn't slip off.

• displacement of the patella from the normal position of the trochlear sulcus
• medial more common
• quadriceps can't extend with stifle out of place.  Not too painful. Can cause lots of pathology. 
• gait: "skip" vs bowlegged vs knock-kneed (LPL)

• I: patella can be pushed out manually, no clinical signs
• II: spontaneous luxation, hopping or kicking.  Surgery if getting worse
• III: out but can be pushed in.  Bow-legged. Surgery if bad or getting worse
• IV: out and can't be put back in. Early sx to prevent deformity!

• conservative for up to III with minimal clinical signs
• Surgery for young developing deformities or progressing or concurrent CCL rupture
• deepen trochlear groove
• tibial tuberosity transposition or suture to keep quads aligned
• release of medial soft tissue
• tighten lateral soft tissue fascia.

• rare
• prognosis guarded
• more in large breeds than small

• common in small dogs
• chronic lameness
• acute progression

disease of synovial joints characterized by inflammation, cartilage degeneration and bony remodeling. Clinical signs of joint pain and physical disability

• injured chondrocytes produce inflammatory mediators (IL-1, TNF-alpha)
• increase production of degradative enzymes
• disrupt normal relationship of collagen and proteoglycans in articular cartilage
• degredation faster than production. 
• collagen destabilizes and stops crosslinking, absorb more water and can't work as well
• surface becomes pitted and fissured, subchondral bone thickens, stiffness and thickening of joint capsule
• bone remodeling and osteophytes cause further damage

• Prefers up stairs to down = elbows
• prefers down stairs to up = hind end

• soft tissue enlargement, osteophytes, bony proliferation and remodeling
• requires ~30-40% change in bone density to see radiographic change
• look for soft tissue (not good for shoulder or hip)

• pain and loss of function are goals
• body weight reduction: 1-2%/week
• exercise modification: activity is necessary, but don't exacerbate lameness.
• anti-inflammatory drugs: NSAIDs PRN
• slow-acting, disease-modifying agents

• block COX1 (constitutive) and COX2 (inducible). COX2 selective preferred.
• Inhibit angiogenesis and gastroprotective PGs
• COX-2 selective: carprofen, meloxicam, robenacoxib/onsior
• COX-2 specific: deracoxib, firocoxib

• COX-2 selective NSAID
• analgesic, antipyretic, anti-inflammatory
• minimium GI toxicity.
• idiosyncratic hepatic toxicity

• COX-2 selective NSAID
• analgestic, antipyretic, and anti-inflammatory
• half dose in cats

• Highly COX-2 selective
• efficacy is higher without food

• COX-2 specific
• maybe not as safe as COX-2 selective

COX-2 specific

• tramadol
• oxycodone
• codeine
• buprenorphine

• reset wind-up phenomenon
• ketamine (CRI for hours, dose-dependent dysphoria)
• amantadine (takes time to show effect)

• gabapentin, pregabalin
• exact mechanism unknown
• neuropathic pain action thought to involve voltage-gated N-type calcium channels.

• support (or don't suppress) chondrocyte synthesis
• inhibit degredative enzymes in articular cartilage
• stimulate (or don't suppress) hyaluronan synthesis
• take a long time--no immediate effects
• polysulfated glycosaminoglycan (Adequan), glucosamine/chondroitin sulfate (cosequin), glycoflex, flex-N-free, pentosan polysulfate (Cartrophen), hyaluronan

• highly-sulfated glycosaminoglycans (mostly chondroitin sulfate
• extracted from bovine lung and trachea
• slow-acting disease modifying agent
• incorporated into CT, inhibits catabolic activity in articular cartilage (protective), upregulates collagen. 
• Best used early in disease.

• slow-acting disease modifying agent
• from bovine CT
• dasuquin is different because it has avocado /soybean
• reduces catabolic and pro-inflammatory mediators
• provide building blocks and stimulates synthesis
• inhibits degradation enzymes

• fibrous: outer, joint stability and flexibility
• subsynovium: source of synovial fluid
• inner synovial lining: type A are m"Acrophage"-like. Type B are fibro"Blast"-like that produce hyaluronic acid

• synoviocytes: modify synovial fluid, scavenge large molecules, nutritional support for articular cartilage
• synovial fluid: ultrafiltrate of plasma with HA. Nourishes articular cartilage, boundary lubricant for periarticular tissues

• lameness
• reluctance to walk
• difficulty rising
• stiff/stilted gait
• joint swellings
• fever
• lethargy
• weakness
• weight loss
• inappetance
• vomiting
• diarrhea

• HISTORY: drug, vax, travel, illness
• non-regenerative anemia, neutrophilia, hypoalbuminemia, increased ALP, proteinuria
• urine culture or UPC
• infectious disease testing: 4dx, RMSF, Lepto, blood culture
• joint rads (erosive from non-erosive), esp carpus
• ANA for immune
• synovial fluid collection: arthrocentesis in 3 joints.  Fluid analysis/cytology = EDTA, smear (hair dryer), C/S

• should be clear and pale yellow, >0.5mL (>1mL abnormal)
• front carpus, back tarsus or lat stifle (bend, needle in the dippy place)
• serosanguinous: blood contamination or joint pathology
• xanthochromic: yellow-orange, prior hemorrhage
• white or light yellow: increased nucleated cells (inflammation, sepsis, neoplasia)
• turbid: increased particulates (RBC, WBC, infectious, fibrin, neoplastic, crystals
• viscosity: 1 inch string test, reduced suggests synovial damage, dilution, degradation of HA. 
• fluid analysis: 1.5-3 protein, <3,000 nucleated cells/uL, mostly mononuclear. Neutrophils in polyarthritis.  proteinaceous background and windrowing/lines are normal
• ragocytes in inflammatory/immune-mediated: neutrophils with round purple variable cytoplasmic granules
• LE cells in SLE: phagocytes with engulfed degenerate pink nucleoprotein

• Trimethoprim sulfa most common (potentiated sulfonamides)
• Pheno, penicillin, cephalosporin
• Large breed, esp black and tan breeds. 
• signs resolve within 2-7d of discontinuing drugs (no need for steroids
• start 12d after first drug exposure or 1h-10d after reexposure.

• Erosive: very rare, subchondral bone destruction (irregular joint surfaces, narrowing or widening of joint space, punched out lesions along joint surface). May take 6 months to show on rads. Rheumatoid Arthritis. 5/10 suggestive, 7/10 diagnostic. poor long term px
• non-erosive: more common, young adults, esp females. Sporting dogs and large breeds (lab, golden, GSD, cocker, eskimo).  4 types (idiopathic, reactive, enteropathic, neoplastic). Fair to good long term px

• Type I: idiopathic. Most common. Dx of exclusion
• Type II: Reactive (infectious or inflammatory disease distant from the joint). Second most common
• Type III: Enteropathic (GI or hepatic, gut barrier causes immune complexes)
• Type IV: neoplasia remote from joint, causes immune complexes

• GSD, sheltie.
• Multi-systemic immune mediated disease. Unknown trigger
• uncommon
• 2-4yrs
• Type II, III, IV aberrent immune responses
• poor px

• inherited auto-inflammatory disorder
• increased HA produced (wrinkles) by dermal fibroblasts, degradation causes fragments seen as Ag, cytokine storm (systemic inflammation)
• recurrent inflammation and high fever for 24-36h. Swollen muzzle, v/d, abdominal/back/joint pain, swollen hock syndrome
• can cause amyloidosis of liver, kidney
• genetic test
• colchicine to prevent collagen formation and fibrosis

• Give idea of improvement or progress, grade (rechecks)
• ability to rise from a down position
• minutes at X speed on a treadmill/walk
• seconds of 3 limb weight bearing before fatigue
• ability to circle tightly
• step over cavaletti rail at x heights

• must be safe
• must be willing
• positive reinforcement
• increase frequency before duration (10-15%/week?).  Back off if lameness after

• perterbation: weight shifting, balance disc/wobble board
• foot placement: cavaletti, obstacles, balance board, uneven or soft surfaces, circle, hip stretch, figure 8
• core balance: 3-legged standing, hemi-standing, hup, box standing

• hill walking
• stair climbing
• treatmill
• wheelbarrow
• dancing
• sit to stand
• hup position and balance
• down to stand
• abdominal crunches
• tunnels
• over to under
• tug of war
• walking backwards downhill

• swim
• underwater treadmill
• incline or decline walking
• cavaletti rails
• dancing or wheelbarrow
• stairs
• handshaking

• ID deficits and limitations
• create goals
• choose therapeutic exercises
• reevaluate patient
• ID deficits and goals

• location/joint: all limbs, shifting. UP the front and DOWN the back
• PE/Hx: Painful lameness, reluctant to rise, sensitive to touch. 5-18mo, usu large breed (GSD), more in males. Pain in long bones. 
• pathophys: unknown etiology, endosteal or periosteal new bone formation. Infection? Stress? 1st heat. 
• rads: 10 days after pain. Wide nutrient foramen, blurring trabecular followed by periosteal and endosteal proliferation. Patchy or modeled bone within medullary canal. Thumbprints.
• tx: time (90d), NSAIDs for pain, NOT steroids. Correct Ca/P ratios

• PE/Hx: lg to giant breed, 3-5 months, acute onset, elevated temperature, pain, metaphyseal swelling. Recumbent.
• pathophys: cause unknown. Not vit C, D, minerals, calories.  Maybe Vit C metabolism?
• rads: periosteal proliferation, double physeal lines, metaphyseal lucency
• tx: supportive, no vit C or D. Pain meds (NSAIDs, Tramadol)
• px: good, watch for growth plate bridging causing angular limb deformity

• location/joint: Usu distal ulna, distal radius and other long bones can be affected
• PE/Hx: large breed, 3-4mo, esp with excessive Ca. Insidious onset of lameness and valgus
• pathophys: delayed formation of bone by a physis due to defect in endochondral ossification - hypertrophied hyaline at core.
• rads: lame shape, sclerotic bone line at metaphysis
• tx: none
• px: primary growth retardation

• location: medial compartment vs lateral compartment (lateral humeral condyle, radial head, lateral coronoid process)
• PE/Hx: stiff, inward elbow and supinated paw, pain on hyperextension/flexion ("cubital test"), joint effusion ("balloon" under anconeus muscle. CAN BE BILATERAL
• pathophys: fragmented medial coronoid process, OCD, incongruity, ununited anconeal process
• rads: look for ununited anconeal, arthritis, incongruities >2mm. May see OCD, fragmented coronoid (may be invisible)
• tx: dietary control of growth, weight control, exercise moderation, NSAIDs, chrondroprotective agents.  Sx before 2y? Arthrotomy or arthroscopy. Unload medial compartment in incongruity (dynamic ulnar cuts)
• px: OA will progress. Do well post-sx if young

• location: CONVEX surfaces, shoulder most. Also distal humerus, stifle, hocks. may be shifting leg lameness. BILATERAL
• PE/Hx: intermittent lameness in young large breed. pain on extension or flexion, muscle atrophy, decreased ROM, OA in adults, crepitus, effusion, periarticular swelling.
• pathophys: endochondral ossification leaves cartilage in physis or articular epiphyseal complex. Cartilage thickening = less nutrition, necrosis, cytokines, may crack.
• rads: Flattening of convex head of bone, line, lucent divot? 
• tx: remove flap, curette down to bleeding bone. Fibrocartilage formation in defect. Could do unicompartment elbow replacement, synacart, osteochondral autograft. OATS = transfer of healthy articular cartilage to OCD lesion.

• stabilizers of diarthrodial ball and socket joint: ligament of the head of the femur, joint capsule, dorsal acetabular rim.  Luxation occurs when two are gone. 
• secondary stabilizers: acetabular labrum, hydrostatic pressure within joint, periarticular muscles (gluteals, iliopsoas, quads, gemelli, internal and external obturdator)
• developmental defect characterized by malformation and laxity (dynamic or functional subluxation)

• signalment: any age/sex/breed. 4-12mo = bunny hopping from laxity. improves at 1-3years when joint capsule thickens. later = OA, stiff and sore esp after exercise. 
• Heritable, but quantitative so hard to control.
• Ortho exam: limited/painful ROM, touch trochanters and sway (feel subluxating hips), ortolani manuver (sedated in lat).

• rads - great for secondary OA, bad for puppies, mildly affected.  
• FHC: want 50% femoral head coverage, careful of "straight" rads because can corkscrew femoral head in
• Norberg angle: line between femoral heads, angle to cranial acetabular rim. Want >105 degrees
• Morgan's line: circle completing femoral head-ish, = osteophytosis of femoral neck:
• Could see (sub)luxation, osteophytosis, flattening of femoral head, in-filling of acetabulum.  
• Check for MUSCLE MASS atrophy: which side is more lame?
• PennHip: measures lateral passive hip laxity. <0.3 or 0.4 distraction index
• Dorsolateral subluxation: drop knees down in hole. >55% is good.

• medical mgmt: weight reduction/maintenance, controlled exercise (PT!), NSAIDs and analgesia (gaba, tramadol, amantadine), disease modifying osteoarthritic agents (DMOA)
• preventative sx: juvenile pubic symphosiodesis (with laxity and OA, 12-22wks), double/triple pelvic osteotomy (TPO) (<10mo, laxity but no OA)
• salvage sx: total hip replacement, femoral head and neck osteotomy (FHO)

• prophylactic sx for hip dysplasia
• 3 cuts, rotate acetabulum over femoral head so it can't slip dorsally
• decrease laxity, normalize articular stress, improve hip joint congruity
• for immature, affected dogs. No joint laxity or OA yet, must have SOME coverage of femoral head (or continue to subluxate). 4-6 wks apart if bilateral
• great prognosis unless secondary OA (which means we chose the wrong P, rads too insensitive)
• complications: damage to sciatic (walk on dorsum of foot), screws pull out/loosen, obstipation and dysuria from pelvic canal narrowing, overrotation decreases femoral neck mvmt = ROM.

• surgically induced premature closure of pubic symphysis with cautery. Pelvic canal stays narrow.  Acetabulum/pelvis can't grow OUT so grows OVER.  
• CASTRATE - will pass as no dysplasia. 
• for P with palpable laxity (too severe will progress regardless). No benefit >22wks (12-22). 
• put your finger under pubis so you don't cauterize the urethra! Cautery until it bubbles.
• will not eliminate joint laxity or OA, but decreases formation.

• palpation: jugular, muscle, tendon (bursa), bone, joint.  Every Cow Loves You (Extensor carpi radialis, common digital extensor tendon, lateral digital extensor tendon, ulnaris lateralis)
• flex - start on sound leg
• HOOF TESTERS
• walk, job, lunge, flex
• rider

hock, stifle and hip

• 0: not perceptable
• 1: difficult to perceive
• 2: apparent under some circumstances (surfaces, inclines etc)
• 3: consistently observable at trot
• 4: obvious at walk
• 5: minimal weight bearing

• Hx
• PE (TPR)
• HOOF TESTERS

• visual gait exam: where is it now? Need help getting up? Hug the wall? Straight lines and circles. "down on Sound", "hip hike", toes spread
• standing exam: symmetry, joint effusion, "long femur disease"
• recumbent exam: CREPI in each joint, ROM, ligament stability (collaterals, cruciate, directional mvmt)

• patella, fabella
• tibial tuberosity, head of fibula
• throughout ROM (partial tears!)

• cup distal femur with leg at standing angle (but P in lateral)
• place index finger from patella down patellar tendon onto tibial tuberosity
• flex hock WITHOUT allowing stifle to flex
• for complete tears of CCL

• weak flexor tendons, congenital usu, from premature vs systemic illness vs lack of exercise. Can be induced from casts etc
• Signs: walking on heels, no weight on toes. Could walk on fetlocks. Hindlimbs more common
• Hx: newborn
• Tx: trim heels flat, heel extension shoes for severe (plantar/palmar support and protect fetlocks/heel bulbs).  Exercise.  Good px

• contracted tendons cause persistent hyperflexion. Fetlock (SDFT, DDFT), carpus (SDFT + DDFT, carpal fascia).
• Signs: knuckling, forelimbs usu, only one joint (coffin, fetlock, carpus).
• Hx: congenital or acquired
• Tx: exercise, oxytet (allows relaxation), NSAIDs, splints, toe extension shoes, surgery in severe (need help to nurse).  Px better if early and can manually straighten.

• acquired flexural deformity: contracted tendons cause persistent hyperflexion/knuckling in coffin (DDFT)
• Signs: unilateral or bilateral. 4wk-4mo.
• Stage 1: dorsal hoof wall less than vertical (better px)
• Stage 2: dorsal hoof wall over vertical, guarded px
• Hx: 4wk to 4mo. Chronic pain in affected limb, rapid growth (caused)
• Tx: diet change, exercise, toe extension shoes, NSAIDs, sometimes oxytet
• sx: distal check ligament desmotomy. Stage 2 may need DDF tentotomy.

• contracted tendons cause persistent hyperflexion in fetlock (SDFT, DDFT, usu both)
• Signs: knuckling on unilateral or bilateral fetlock joint with hoof at normal alignment
• Hx: acquired, 9mo-2yrs.  Chronic pain in affected limb, rapid growth (cause)
• Tx: diet, exercise, toe extension shoes, NSAIDs, sometimes oxytet.  Splinting. 
• sx: proximal +/- distal check ligament desmotomy, rarely SDF tenotomy.

• lateral (valgus, knock-kneed) or medial (varus, bow-legged) limb deviations below a joint. VIEW FROM FRONT
• Carpal valgus, fetlock varus
• Can be carpus, fetlock, tarsus. forelimb more common than hind.
• Hx: born straight, crooked in weeks/months from growth plate injury, physitis, contralateral lameness, rapid growth, incomplete ossification (sickle hock and carpal valgus)
• Tx: sleeve cast for 14d that ends at fetlock for incomplete ossification (tx EARLY).  Otherwise conservative (rest, trimming, shoes)
• Sx: for moderate/severe at end of physeal growth. periosteal transection on concave side to stimulate growth, transphyseal bridging on convex side by tying screws together to slow growth (remove when straight), single transphyseal screw from above to below physis (remove when straight), wedge osteotomy
• ALPACAS ALWAYS HAVE CARPAL VALGUS

• lateral (valgus, knock-kneed) or medial (varus, bow-legged) limb deviations below a joint. VIEW FROM FRONT
• Carpal valgus, fetlock varus
• Can be carpus, fetlock, tarsus. forelimb more common than hind.
• Hx: born crooked
• Tx: congenital may correct alone (windswept where both legs go in same direction due to ligament/tendon laxity, controlled exercise)

humerus

straight line can be drawn through the bones of the hoof through the fetlock, no need to change angles at pastern (broken back like thoroughbreds with no heel or broken forward like clubfoot)

perform the lameness exam BEFORE pulling the shoes!

• USE THEM!  Channel lock allows adjustment while handles are still small enough for 2 hands on both
• 1: top and sole at toe
• 2: top and sole laterally at level of tip of frog
• 3: sole (frog to outside) in the back
• 4: across heel bulbs
• 5: frog to top at midline
• 6: frog to outside laterally (inc frog!)

• etiology: poor riding surface, thin-soled horse.
• signs: variable lameness, visible bruising on sole surface, sensitive to hoof testers
• tx: full pads when shod, paint sole with iodine. Dry out foot and protect!
• Corns: when bruises are at angle of wall and bar.  Due to bad shoeing or shoe on too long.

• infection of lamina, sensitive.  Gravel = abscess drains at coronary band
• etiology: sole trauma, laminitis
• signs: acute, severe lameness, reaction to hoof testers
• tx: debride, soak, protect from contamination, rads to R/O laminitis.  Don't use epsom salts!  Dries out--you want the foot soft so the abscess can burst.  THEN dry it with salt.

• Infection/necrosis in frog area (check sulci)
• etiology: poor environment
• tx: change environment!  Clean feet daily.  Topical therapy.

• horn hypertrophy (overgrowth). Draft horse disease
• more hind than front
• lameness if the frog is involved
• tx: routine foot care, change environment as needed, debride, abx

• fissures in hoof wall, usu parallel to laminae.
• +/- lameness, infection
• Toe/quarter cracks: start at bottom, good px
• coronary cracks: start at coronary band, caused by previous injury.  Poor prognosis
• Tx: patch, hoof resection, shoe

• non-neoplastic, smooth growth of horn (inward), seen on rads.  Usually in toe region
• don't mistake crena - normal ratty divot at center of toe.
• +/- lameness
• tx: remove affected hoof wall and debride all abnormal tissue.  BLEED

• widening and change of horn substance at white line
• etiology: torn lamina vs chronic laminits
• SEQUELA

• infection in separated hoof wall - bacteria, fungus, yeast
• Tx: hoof care!  +/- abx, antifungals.

• calcification of collateral cartilages from HARD impact on feet.  Just cartilage (ignore!)
• rarely causes lameness

• necrosis of collateral cartilages
• moderate lameness
• Try to get all the bad out, but never seem to manage it.

• chronic remodeling of P3
• etiology: concussion, thin soles
• diagnosis: radiology
• Rule out P3 infection (puncture?)
• Tx: decrease training, sole protection (rim pad? Get the soles off the ground!), paint with iodine to toughen.  Stem cells may work but $$$

• IS AN EMERGENCY
• maybe leave nail in for radiographs, but you never know where it's going!  
• Rads with probe and contrast.  Navicular = death because of bursa.
• What matters is how quickly you treat!!
• Ice the other side -- contralateral laminitis

• toe ulcer to necrosis at tip of LATERAL claw.  
• Can progress to necrosis of the apex of the distal phalanx
• affected toe is overgrown, excessive wearing of heels to try not to walk on it
• conservative tx: trim hoof growth, orthopedic block on healthy claw to get weight off
• surgical tx: amputation of digit and removal of necrotic bone (partial = curette)

• non-infectious: Most economically important, 40%. Chronic disease with multi-factorial causes. overgrown/deformed, sole ulcers, white line
• non-infectious: thin soles, new barn disease
• infectious: foot rot, hairy heel warts, interdigital dermatitis

• soft tissue inside sole damaged, normal horn can't be produced.  Corium or "live" tissue is exposed. 
• causes: physical pressure, physiology/metabolism (calving, illness, diet)

• separation between sole and hoof wall.
• Infection can enter through gap

• complex structure of mostly adipose under distal phalanx
• dampens compression of corium
• BCS 1.5 and below have very thin digital cushions, and bad cushions = lameness. 
• Non-lame cows produce WAY more milk than lame cows.

2/3 in lateral, 1/3 in medial.

• restore balance between inner and outer claws to prevent pressure induced lesions
• correct toe length to get correct sole depth, so P3 is parallel to the ground.  Spare the heel!
• Heel of medial claw is lowest point, reference for entire foot

• M1: subclinical, <20mm breakdown of skin
• M2: >20mm, acute clinical stage. "strawberry dermatitis", clean and rub dry. Abx curative. Don't bandage!
• M3: healing stage
• M4: chronic stage. Tend to recur, dormant lesions reborn (M4.1 returns to M2)
• Rumen may be potential reservior

• interdigital skin punctured and fusobacterium necrophorum infects interdigital space
• rapidly painful and swollen, pushes digits apart. Tx with systemic abx

• closest to dorsal or lateral-most surface
• Ball bearings show the direction of gravity

• dorsal
• dorsomedial
• dorsolateral
• medial
• palmaromedial
• palmar
• palmarolateral
• lateral

• surface you see in PROFILE
• vs
• **How the xray beam passes through the patient (entry to exit) (dorsolateral shows ventral and medial in profile)

dorsolateral and palmaromedial surfaces in profile

lateral and medial in profile

dorsal and palmar in profile

• "I goes high"
• intermediate carpal bone is higher, medial drops down

lateral

proximal and distal sides

proximal and distal

• dorsoproximal-dorsodistal oblique
• shows dorsal, lat and medial in profile

• wide on the DP and narrow on the DL
• on DMPLO, bottom right makes a "+", on DLPMO it makes a "T"

• DMPLO: bottom right has a "C" shape
• DLPMO: the three bumps at top of joint, two Cs in the middle opposite calcaneus. Bottom right is bigger and blocky

can't tell, need the label to be correct

• failure of endochondral ossification causes growth of cartilage, causing vascular failure, ischemic chondronecrosis
• could be caused by genetics (growing too fast), nutrition, bacteremia, excessive exercise

• "physitis, epiphysitis"
• usu distal radius during growth spurt in fast growing
• signs: variable lameness, enlarged physes (tender to palpation)
• rads: wide, irregular physes, metaphyseal flaring
• tx: NSAIDs, rest (none - self-limiting)
• px: good

• synovitis (effusion).  +/- lameness (esp after work/flexion). Eventually leads to OA
• synovitis +/- lameness are more dramatic with free fragments (dissecans), not related to prognosis

• convex surfaces
• femoropatellar: lateral trochlear ridge, patella
• hock: distal intermediate ridge of tibia (DIRT), lateral and medial trochlear ridges of the talus, medial malleolus
• shoulder: humerus, glenoid
• metacarpo(tarso)phalangeal: sagittal ridge and condyles of MCIII/MTIII
• cervical vertebrae

• 1-8y
• quarterhorses (conformational predisposition)
• signs: effusion, variable lameness, positive flexion tests
• tx: arthroscopy, debride, graft or just put a screw through it

• insertion of short distal sesamoidean ligament on P1
• avulsion fractures, no evidence of cartilage/OC
• standardbreds
• arthroscopic fragment removal and debridement

• clinical in one joint, radiographic bilateral.
• +/- effusion
• more in males
• stifle>tarsi>carpi>shoulder>digit
• most with concurrent OA
• SX NECESSARY

• common and debilitating
• flexors>extensors, SDF>DDF, forelimb>hindlimb, L more than R
• slow to heal, doesn't regain elasticity and strength, recurs
• classes: external (laceration, trauma) vs internal (overload, hyperthermia, vascular), intrasynovial (poor px) vs extrasynovial (better px)
• causes: altered conformation (under-run heels, long toe), hard or soft ground, muscle fatigue near end of performance
• phases: Pre-clinical, clinical (1-2wk, inflammation), repair (peaks 21d after signs, angiogenesis), remodeling (up to 18mo)
• signs: visual "bow", lame, inflammation
• tx: REHAB! ACTIVE REST, time

• smaller cross-sectional area
• more external so greater strain and trauma
• less vascular in mid-metacarpus

• transection of the accessory ligament of the SDFT
• increases elastic length of muscle/tendon unit in bowed tendon/tendonitis
• palmar/plantar annular ligament transection for long bows (more room for SDF/DDF to move/heal/function)

• ALWAYS AN EMERGENCY
• extensor heal well
• flexor extrasynovial heal okay
• intrasynovial don't heal as well
• INFECTION IS LIFE THREATENING
• contralateral laminitis

• fibrosis of semitendinosis (and semimebranosis)
• unilateral usually
• trauma (butt bar, kicked etc)
• dx: characteristic gait - moonwalk.  U/S, rads
• Tx: semitens tentotomy

• neurogenic (dandelions in Australia)
• tx: lateral digital extensor myotenectomy
• GOOSE STEP, not painful, not sure why.  One leg VERY picked up

• anti-inflammatories
• hoof care and support
• cryotherapy
• manage underlying

• we don't know why (concussion? insulin resistance? ischemia?) but there are precipitating events
• inflammation of sensitive laminae and breakdown of union with SENSITIVE laminae of P3 and INSENSITIVE laminae of hoof wall
• signs: forelimb lameness with bounding pulses and sensitivity at toe with hoof testers, rocked back stance, heat over dorsal hoof wall, softening at coronary band (ooze), distal phalanx rotating through sole (crack, soft area, drainage at apex of frog)

• endotoxemia: diarrhea, pleuropneumonia, colic (strangulation, colitis, enteritis), septic metritis/retained placenta, grain/CHO overload
• mechanical overload: contralateral/support limb laminitis
• equine cushings: PPID changes glucose metabolism?
• EMS: insulin resistance
• corticosteroids
• black walnut

• developmental: initial causative insult
• acute: appearance of clinical signs
• subacute: begin after horse has been lame with laminitis for ~72h
• chronic: digital collapse (rotation or sinking) but foot stable

• baseline and progression for 5-7d
• signs: rotation of P3, sinking of P3, increased dorsal hoof wall thickness, hoof wall separation, remodeling of toe of distal phalanx
• lag behind clinical signs
• lateral to medial with horse on a block (ideal), mark dorsal hoof with radiopaque

• cryotherapy (cold = vasoconstriction, during developmental phase)
• anti-inflammatories (flunixin, bute, firocoxib, doxy, NO STEROIDS)
• treat underlying
• hoof care (remove shoe, palmar support like styrofoam, trim toe, special shoes)
• stem cells
• supportive
• digital blood flow therapy (pentoxyphylline, ace. Stem cells?)
• surgery (DDF tentotomy at mid-cannon or mid-pastern, or dorsal hoof wall resection for abscesses
• euthanasia

• vascular: altered blood flow to/from navicular region
• biomechanical: degenerative changes from increased mechanical forces on navicular bone and ligaments (DDF, supporting ligs)

• excessive body weight
• small feet
• upright pastern angles
• hoof imbalances
• work on hard surfaces (concussion)

• pain: intraosseus pressure, damaged soft tissue, bursa
• location: palmar 1/3 of foot (perineural, coffin joint, navicular bursa). Unilateral or bilateral, asymmetric lameness (progressive and chronic), can have extensor muscle atrophy

• stiff and shuffling, won't stride out
• low heels, under-run heels, broken back hoof pastern angle, medial-lateral hoof imbalance, small upright foot, narrow foot, contracted heels, sheared heels
• +/- sensitivity to hoof testers across heels, frog and possibly toe

• variable lameness
• typically bilateral but asymmetric (one more severe than other)
• stiff, shuffling, choppy gait
• short cranial phase of stride
• Tend to land on toe
• lameness exacerbated by hard surface, lower limb flexion, wedge test, frog pressure, working in circle

• small volume with small gauge needle
• desensitizes caudal 1/3 of foot and sole
• show marked improvement (80-90%)
• majority "switch over" after blocking

intra-articular anesthesia of coffin joint is NOT helpful in differentiating problems of coffin and navicular

• remove shoes
• clean feet
• pack with play-doh (remove air artifacts)
• bilateral!
• lateromedial: see proximal and distal (palmar angle (bone to hoof)
• dorsoproximal-palmarodistal: increase in number, size and abnormal shape of synovial invaginations
• palaroproximal-palmarodistal (tangential or skyline): erosions in flexor cortex, corticomedullary distinction (fuzzy)
• flat dorsopalmar: medial to lateral hoof imbalance
• loss of corticomedullary distinction, medullary sclerosis, mineralization of deep digital flexor tendon, enesthophytes

• fracture of navicular bone
• rupture of DDF

• rest + light work
• corrective trimming and shoeing (egg bar shoe, shorten toe, raise heel)
• anti-inflammatory (bute, IA steroids, HA, PSGAG)
• drugs for arthritis (isoxsuprine hydrochloride, beta-adrenergic; pentoxyfilline to decrease inflammation, bisphosphanates to decrease bone resorption
• meds to improve blood flow
• palmar digital neurectomy (lasts 2yrs, not ideal)
• suspensory branch desmotomy (reduces force on navicular)

• common forelimb lameness
• typically bilateral but asymmetric
• localized to palmar 1/3 of foot
• dx with clinical signs, response to local and imaging
• lots of tx options
• corrective shoeing to restore foot balance and reduce forces on navicular region

• salvage procedure - appropriate hemostasis, tissue handling (gentle!), wound closure (no tension!), analgesia. Ligate vein before artery
• scapulectomy, forequarter, mid-humeral, coxofemoral, mid-femoral, digit
• "Tripawds.com"

• salvage procedure when amputation not an option.  Bone removed, Thick strong plate attached across as bridge
• tumor/injury must be located in appropriate place
• Expensive and LOTS of complications

• surgical fusion of a joint to form bony ankylosis
• complete loss of motion at affected joint.
• alleviates pain
• for irreparable fracture, chronically unstable, severe DJD, neuro injury (though must know where foot IS)
• remove articular cartilage, angle joints properly.  Rigid, long-lasting fixation + bone graft. External cast/splint for support.
• tarsus, carpus, shoulder. Stifle, elbow, digits

• salvage for hip dysplasia when pain/lameness can't be alleviated, not a candidate for THR
• REQUIRE PT, DO NOT CAGE REST. Analgesia.
• Will still be lame, comfort is the goal

• salvage for OA, hip dysplasia, pain, lameness, lost function, low QOL
• complications: luxation, femur fx, infection, aseptic loosening
• most return to normal function
• must be skeletally mature, good BCS, can be cage rested, no luxation. Expensive
• Prosthesis goes down femur, lateral bolt stops slippage (subsidence). Many implant choices
• hematogenous infection a lifelong risk.

NOT good - 50% catastrophic failures

for conditions we can't effectively treat, after you've tried EVERYTHING else

• MC/CT2 and 4
• from external (kick, skin infection, sequestra (necrotic bone), tendon/suspensory damage) or internal (pressure from suspensory desmitis, proximal sesamoid bone damage
• forlimbs>hindlimbs
• check suspensory before tx
• distal 1/3 = remove (too much and rest will luxate.  Prox 1/3 = sx fixation.  No implant if communicates with joint.  too much callus will impinge on suspensory ligament

• 7 classifications, what matters is ARTICULAR OR NOT.  VII is only in foals, no tx
• dx via hoof testers, nerve blocks, rads. 
• non-articular: rest, shoe, neurectomy. Good px
• articular: extensor process is only one with good px (remove arthroscopically). Rest need screw, shoeing, salvage. Poor to fair px

• fatigue failures from inappropriate training, microfractures from bone remodeling too fast
• "bucked shins" in early phase - no fx but sub-periosteal callus
• dorsal MC3 fracture ("saucer" - cortical) later. 
• Distal MC3/MT3 fractures later - Condylar, fetlock.  Lame by the time off track.  Effusion, sore.  MEDIAL CAN SPIRAL, lat more common
• Fix with lag screw to prevent displacement. Distal screws can stay in

• intra-articular fx.  Cause recurrent synovitis, OA, shortened athletic. Usu in racehorses. 
• "knee chips" (carpal hyperextension).  Distal radiocarpal bone, distal intermediate carpal bone, proximal third carpal bone.  
• effusion/lame when cooling, OK within 24-48h, recur with exercise. 
• rads: 4-6 views of EACH carpus - often bilateral. Lat, flexed lat, DP, DLPMO, skyline
• tx: arthroscopic sx, chip removal vs fragment repair, debride
• px: good for acute and <30% of cartilage lost

intermediate carpal bone (so you can tell radiocarpal from intermediate carpal

• hyperextension fractures
• RF medial eminence P1 (bilateral)
• present and tx like carpal, but less cartilage damage so better px
• effusion/lame when cooling, recur with exercise, tx via arthroscopic sx. Chip removal or slab repair

• 6 types, px decreases as goes distal - only apical and abaxial good px
• assess suspensory desmitis!!
• joint effusion, heat, pain on palpation, variable lameness
• tx: arthroscopic removal vs repair (lag screw better than wire). Or retire.

• can lead to loss of suspensory apparatus!  Stabilize or will stretch neurovascular and cause thrombosis etc. Immobilize ASAP!
• no chance of return to function

chips only communicate with one articular surface, slabs communicate with two

• EMERGENCY
• tx fast to avoid OA
• foal (px worse) vs adult
• non-hematogenous: pucture, contiguous soft tissue (E)
• Hematogenous: SEPTic
• S = synovium
• E = epiphysis
• P = Physis (physeal vessels, premature closure of physis, angular limb deformity)
• T = tarsal bone (premature foals, joint collapse and angular limb deformity)

• hematogenous rather than penetrating
• prematurity, umbilical abscesses, FPT.  Usu <1mo
• FOALS ARE FEBRILE (adults are not)
• type T (tarsal bone from not ossified yet) and P (physis) can cause angular limb deformity
• 60% have concurrent osteomyelitis/bone necrosis on rads

• cytology/gram stain in EDTA or heparin
• Culture in blood culture vials
• should be translucent yellow, viscous.  CLoudy suggests >30,000 cells

• synovial fluid cytology (neutrophils)
• gram stain (we suck at culturing, so no growth does NOT mean not infected)
• serum amyloid A not specific to sepsis
• Rads: lytic changes in 1 week (lag). Look for gas opacity. 60% of foals have concurrnt osteomyelitis/bone necrosis

• eliminate infection: Local abx via IA or IV regional limb perfusion, intraosseus (necrotic bone), abx implanted beads (longest, cattle). Systemic abx?
• establish drainage: arthroscopy, arthrotomy (scars). Balanced solution. DILUTION
• analgesia: pain meds, reduce contralateral laminitis
• Restore joint milieu: HA, bandage, PT

shape of the bones of the fetlock joint.  Dorsal looks like lips and palmar/plantar surface is the whale tail.

• tarsus: distal intermediate ridge of the tibial cochlea (DIRT) - DLPMO
• tarsus: lateral trochlear ridge of the talus - DMPLO
• stifle: medial femoral condyle - craniocaudal or CdL-CrMO
• stifle: lateral trochlea of the femur - lateromedial or CdL-CrMO

the joints proximal and distal to the fracture to ensure no involvement

usually image only most severely affected joint or two

• presence and type of periosteal reaction
• presence and type of bone lysis
• zone of transition between normal and abnormal bone (short is either, long is aggressive)
• rate of progression (requires serial, fast is aggressive)
• there are no MILDLY aggressive lesions.  There are aggressive and non-aggressive
• may only require one to be considered aggressive
• aggressive is usually infection or neoplasia

• continuous periosteal reaction: can be aggressive or non-aggressive. Smooth margins and uniform new born formation. CONTINUOUS line. 
• interrupted periosteal reaction: aggressive. non-uniform, disorganized, irregular. You'd have to lift the pencil. Sunburst. 
• tumor new bone formation: aggressive. Irregular, mottled. 
• Reactive new bone formation: normal bone reacting to disease process nearby.  Can be aggressive or not aggressive. Organized, increased opacity, thick normal trabeculae or periosteal reaction.

• 30-50% must be gone to be seen by rads. Mostly care about "present or absent"
• geographic: non-aggressive and aggressive. "globe" lucency, possible sclerotic rim. Could be cyst or abscess
• moth-eaten: aggressive. Swiss cheese. Medullary and cortical
• permeative: aggressive. Collander holes in cortex and medulla
• cortical: aggressive. Beaver-eaten tree?
• Punctate: discrete margins like cookie cutter.  Usu myeloproliferative neoplasms

• monostotic: one bone
• polystotic: multiple bones
• diffuse: all bones
• focal: one lesion
• multifocal: multiple lesions with generalized random distribution
• locally extensive: multiple lesions in one area
• usually due to infection or neoplasia

• secondary change in the skeleton due to disease elsewhere in the body - look for underlying!
• palisading or continuous periosteal reaction, esp in diaphysis of long bones of all four limbs.  Usually starts distally and moves proximally. 
• take chest rads first--bronchial carcinoma

cranial displacement of infrapatellar fat pad

periarticular "collar" of new bone at chondrosynovial junction

new bone formation involving insertion of tendons, ligaments and joint capsule away from osteochondral junction

when a joint becomes stiff or fixated due to natural causes

• flattening or concavity of subchrondral bone (makes joint space look wide)
• adjacent sclerosis
• mineralized cartilage flap
• articular calcified body

OCD is when the flap breaks off

focal "thumbprint" increased medullary opacity, in one or many bones

• double physeal lines
• periosteal reaction

• failure of bone following a force that by itself is insufficient to cause bone failure
• insufficiency: normal stress applied to abnormal bone - more often called pathologic fractures than stress
• fatigue: normal bone subject to repeated stresses that are eventaully enough to produce fracture leading to failure.