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Lecture 1Wednesday, May 14, 20089:31 AM Key to colors/notations
Green highlighted words and phrases represent definitionsYellow highlighted words and phrases represent things Dr. Kuhn emphasized or which seem key to learningA small pen to the left of something (typically a chart) indicates the information is important
Pre test
1. Provide a definition for CTA computerized imaging modality utilizing attenuating X-rays and simultaneous motion of the tube and scintillator to produce a 3-dimensional, variable slice, image of the part imaged
a. Examples of proper useTrauma situations, measurements of anatomical size, enhanced soft tissue resolution over plain film
b. Examples of weaknesses of the toolStarburst artifact of occipital bone, difficulty with imaging near metal implants, high radiation dose, doesn't demonstrate physiology
2. Provide a definition for MRiA computerized imaging modality utilizing induced precession and radio frequency output to produce a 3-dimensional, variable slice, image of the part imaged
a. Examples of proper useSoft tissue imaging, central canal imaging, neural imaging, skeletal survey for tumors, physiology
b. Examples of weaknesses of the toolClaustrophobia, metal implants, expenses, time of exposure
3. List several other imaging toolsDiagnostic ultrasoundBone scan (SPECT)MRAFMRiMyelogramTomogram
4. Define the following and give examples:a. Congenital anomaly=a lesion that an individual is born with
Straight back syndrome, Os Odontoidium (now thought as non-union fracture)b. Normal variant=a different than 'normal' presentation but with no clinical significancec. Dysplasia=congenital anomaly with multiple systems involved, typically has similar risk profile
5. What is the classification system used for soft tissue calcification Physiological Dystrophic Metastatic
Serum calcium Normal Normal Abnormal (high)
Tissue calcium Normal Abnormal Normal
Examples Thyroid cartilageStylohyoid ligamentArcuate Foramen
Calcific tendonitisCalcific bursitisMyositis Officans
HyperparathyroidismLytic MetastasisMultiple Myeloma
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Lecture 2Monday, May 19, 200810:16 AM Arthritis 4 categories of arthritis
Degenerative-DJDInflammatory-RAMetabolic-GoutSeptic joint/Septic arthritide
Terms
Enthesis= musculotendonous attachment of Sharpe's fibersMonoarticular=1 jointPolyarticular=4+ jointsPauciarticular=2-3 jointsOsteophyte=accessory boney growth adjacent to the joint (periarticular)Syndesmophyte=calcification of outer annular fibersSeronegative=no chemical marker within the blood
Poster children
Degenerative-DJD/OAClinical features
Local inflammation is presentMorning stiffness in affected jointsReduced range of motionSwelling of afflicted jointOsteophytic changeMonoarticularChanges in soft tissue contour
Lab findingsNo prominent findings (seronegative)No change in ESR (Eosinophil Sedimentation Rate)Biopsy abnormality
Thinner corticesLowered MMP (methylmetalo protease)Activation of cytokines (pathologic)]
Radiographic findingsDecreased joint space in asymmetric patter(medial worst) owing from decreased articular cartilageSubchondral sclerosis=whitening/thickening of cortical bone underneath articular cartilage
(due to increased stress input from decreased articular cartilage)OsteophytesGeode/subchondral cyst formation (can be synovial fluid or blood or both)
Most commonly seen in large joints (hips, knee, shoulders)Inflammatory-RA
System inflammation is presentMetabolic-GoutSeptic joint/Septic arthritide
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Lecture 3Wednesday, May 21, 20089:19 AM Continued from last lecture DJD=gradual loss of articular cartilage, combined w/ thickening of the subchondral bone; bony outgrowths at the joint margins, and nonspecific synovial inflammation Poster children
Degenerative-DJD/OAClinical features
Local inflammation is presentMorning stiffness in affected jointsReduced range of motionSwelling of afflicted jointOsteophytic changeMonoarticularChanges in soft tissue contour
Lab findingsNo prominent findings (seronegative)No change in ESR (Eosinophil Sedimentation Rate)Biopsy abnormality
Thinner corticesLowered MMP (methylmetalo protease)Activation of cytokines (pathologic)]
Radiographic findingsDecreased joint space in asymmetric patter(medial worst) owing from decreased articular cartilageSubchondral sclerosis=whitening/thickening of cortical bone underneath articular cartilage
(due to increased stress input from decreased articular cartilage)OsteophytesGeode/subchondral cyst formation (can be synovial fluid or blood or both)
Most commonly seen in large joints (hips, knee, shoulders)
Inflammatory-Rheumatoid ArthritisClinical presentation
System inflammation is presentUlnar deviation of MP joints of handsDecreased and painful movementsLots of soft tissue swellingPolyarticular processAlso present in the C-spine, hips, knees, elbowsPannus formationDestruction of the soft tissue surfaces leading to ulnar deviationUsually bilateralSymmetrical joint space narrowing (w/in same joint)Don't mess with when flared up
RA Produces highest number of ankylosis in the handsALL Inflammatory arthritides present danger of ADI instabilityAnkylosis may produce lack of joint motion in all inflammatory arthritidesHyperemia (increased periarticular blood flow) may erode bone and produce osteopeniaLab findings
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Positive rheumatoid factor (usually present)Increased ESRC-reactive protein
Radiographic findingsUlnar deviation1st thing seen: Decreased joint space (symmetrically)Swelling of MP, PIP joints (Bouchard's nodes)No swelling of DIP!!!Periarticular soft tissue swellingPeriarticular osteoporosis Rat bite lesions (produced by pressure erosion and pannus formation)
Metabolic-Gout (will be CPPD)Clinical presentation
Older men predominantlyPredominance of the heels, big toe, thumbAbnormal soft tissue (sticking out), pannusChanges made to the underlying boneNo initial changes in joint spacing/bone makeupPain and redness in area of swelling
Lab findingsTissue/suction biopsyIncreased ESRBlood/urine may be normal or abnormal
Radiographic findingsNo bone changes seen but adjacent soft tissue may calcify (dystrophic)
Septic joint/Septic arthritide
Clinical presentationLots of swelling/painIf younger person they got sick quicklyIf older person they took a while to developDestruction of both joint surfaces will occur in chronic conditionsHot, red, swollen, tender jointsPrevious URTI, recent UTI, or recent skin infection
Lab findingsWBC elevationESR elevation when large joints are involved
Core of ESR measures stability of blood poolIf sampled infectious organism may be present
Radiographic findingsSymmetrical destruction of joint spaceCortical damage
Watch what separates from arthritide Degenerative category
DJD=gradual loss of articular cartilage, combined w/ thickening of the subchondral bone; bony outgrowths at the joint margins, and nonspecific synovial inflammation
GeneralsMost common joint disorder in the worldStriking age correlation
1/3 of all 65 year olds affectedMore common in men vs women younger than 50 (post traumatic/wear and tear)More common in women vs men older than 50 (hormonal changes)
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Predilection for weight bearing joins of the lower extremity, cervical and lumbar spine, and some joints of the hand
EtiologyKnown local factors associated with secondary DJD
WeightInjury
OccupationalRecreational
Skeletal anomaliesQuadriceps strengthKnown systemic factors
Reduction in estrogen levelsGenetic susceptibilityLow vitamin D and C intake
Crystal deposition diseasesHemophiliaPaget'sMost sero - and sero + arthritides
Stages (3)Phase I: Edema and microcracks (enchondral tissue)
Edema of the extracellular matrix, cartilage loses its smooth aspect, and microcracks appearThere is focal loss of chondrocytes, alternating with areas of chondrocytes proliferation
Phase II: Fissuring and pittingThe microcracks deepen in the direction of the forces of tangential cutting and along fibrils of collagenClusters of chondrocytes appear around these clefts and at the surface
Phase III: ErosionFissures cause fragmentation of cartilage to detachThese loose fragments cause the local inflammationThis form of inflammation is much more limited than the typical RASubchondral microcysts form (may develop into geodes later)
PathogenesisThe physiologic homeostasis of normal articular cartilage is driven by chondrocytes, which synthesize collagens, proteoglycans, and proteinasesDJD results from failure by chondrocytes to synthesize good quality matrixThis abnormal chondrocytes synthesis is the result of tissue activation by cytokines, lipid mediators (mainly prostaglandins) free radicals (NO, H2O2) and constituents of the matrix itself, such as fibronectin fragmentsActivated chondrocytes become capable of producing proinflammatory mediators Certain proteinases are involved in the destruction of cartilage
Matrix metalloprotienases (MMPs) are the most potentThe MMPs are held in check by Tissue Inhibitor MetalloProteinases (TIMPs)As long as the MMPs and TIMPs are in balance no degradation occursThe enzyme, aggrecanase, plays a major role in the degradation of the matrix
Although DJD is classified as non-inflammatory arthritis, inflammatory cytokines may stimulate chondrocytes to release cartilage-degrading enzymesLipid mediators, eicosanoids, can activate chondrocytes to increase synthesis of MMPs ,tipping the balance towards degradation Nitric Oxide plays an uncertain role in DJD
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Some studies suggest an ability to induce "DJD, while other studies suggest some protection of the cartilage"
Degenerative
Inflammatory-RA
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Metabolic-Gout
Septic
DJD
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Lecture 4Wednesday, May 28, 20089:14 AM Frequency of Arthritis on radiographs (how often you will see stuff on films)
Weekly Monthly Yearly
DJD Ankylosing spondylitisCPPDDISHOsteitis Condensans Ilii (OCI)Psoriatic arthritisRASynoviochondrometaplasia
Gout infectionLupusReiter's syndromeScleroderma
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Age of onset Arthritis
0-20 years 20-40 year old 40+ years
JRA (Juvenile Rheumatoid Arthritis)/JCA (Juvenile Chronic Arthritis)May be seropositive or seronegative
Ankylosing spondylitisOsteitis Condensans Ilii (OCI)LupusReiter's syndrome/Reactive arthritisPsoriatic arthritisSclerodermaSynoviochondrometaplasia
DJDDISHGoutHypertrophic osteoarthropathyPseudogout (CPPD)
Arthopathies associated with distinct sex predilection
Male Female
Ankylosing spondylitisGoutHypertrophic osteoarthropathyReiter's syndrome/Reactive arthritisSecondary OA
JRA/JCALupusOCIPrimary OARheumatoid ArthritisScleroderma
Reminders of Categories of joints
FibrousStressed Syndesmosis found in Running sports, martial arts, springboard divers
Cartilage joint (disc)Not compartmentalized like always depictedDiscogram does show NP in disc
Synovial jointsVariety of arthritides
FIBROUS CARTILAGINOUS SYNOVIAL
Cranial suturesSyndesmosis (tib/fib, radius/ulna)
Symphysis pubisIVDSternal Angle of LewisSternoclavicularAcromioclavicularJoint Capsules
FingersToesKneesHipsApophyseal jointsSI joints
DJD
Predominates in the spine and in large weight bearing jointsIncomplete understanding of DJDAppears to be an end pointNeed to de-emphasize the -itis (as in arthritis)Local inflammatory reactions Film: Lower Cervical AP
Common radiographic findingsDecreased disc spaceSubchondral sclerosis should be seen
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Sharpening/thickening of uncovertebral joints (1st stage of degenerative stage of Uncovertebral Arthrosis)Remodeling of lateral margin due to altered alignment
Film: Oblique Cervical
Common radiographic findingsShows anterior-lateral osteophytesWatch for
Abnormal IVF (oval with concave edges)Uncovertebral encroachment
Positioning is very important (may appear to have smaller IVFs but may not)
Film: Lateral CervicalCommon radiographic findings
Look at disc spacing (should be even posterior and anterior)Watch posterior elements for sclerosis/thickeningExamine the anterior body and posterior elements for osteophytes
Pt asks "How did my neck get like that?"
Improper wear and tearThe body's process of stabilization of a joint not moving/functioning properly Couch potato story
Large group of patients split in half (homogenized except for activity level)People that are less active get more DJD and wear faster than active group
Rat StudyGenetically identical rats at different agesOlder versions have synovial fluid removed and stuck into younger versionsControls and young versions dissected and experimental rats had local subchondral sclerosis and osteophyte growth after short periods of time
Film: Lower CervicalTypically not symmetricalThis particular film shows uncovertebral hypertrophy (previous "T-bone" style accident)
Film: Proton Density MR imagePosterior vertebral bodies have osteophytic growths
Film: CT Bone window
Shows osteophytes in posterolateral margin of the vertebral bodyFilm: Lateral Cervical
Routinely we will see major changes and alterations in osteophytic growth and/or alterations in lordosis/motion planes
Film: Lateral ThoracicTrue retrolisthesisFacet degeneration definitely presentLoss of disc spaceHuge osteophytesLimited segmental motion
Film: AP LumbarMassive osteophytes on left connecting L5-S1 on leftNone to little segmental motion (can't claim fusion unless we see trabecular fibers bridging the former joint space)May have hook shaped osteophytes between segments
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Film: Lateral LumbarVacuum phenomenon=tearing of annular fibers leading to opening of space and pulling of gas out of solution after the NP dissolvesVacuum cleft=marginal disruption of outer annular fibers (may be trauma related or related to degenerative changes)
Hahn's fissure=midline artery supply and vein drain for vertebral body (shows up on MR)Lower Cervical AP (DJD)
Oblique Cervical (DJD)
Lateral Cervical (DJD)
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Proton Density MR vs T1 MR (DJD)
Lateral Thoracic (DJD)
AP Lumbar (DJD)
Vacuum Cleft
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Lecture 5Monday, June 02, 200810:16 AM DJD
SpondylolisthesisAnterolisthesis
Spondylolysis=fracture acting as causative agent for anterolisthesisSpect or MR scans become indicated if modified Stork Test is positive (localizes pain to one area)
Stork Test/Modified Stork Test=Gillet's TestFacet degeneration=alternative causative agent for anterolisthesisOblique film will allow classification easily (check for pars break)Examine the cortical lines to evaluate for fractureSubchondral sclerosis will compromise the joint space
Film: CT Myelogram-demonstrating neuritis (shown in class)
Shows bone window but cord appears as white dot and cauda equina appears as black dot w/ white border (nerve root inflammation will appear as blurriness)The nerve root sitting against a facet osteophyte is the likely cause of the neuritis (nerve root inflammation) and would benefit quite nicely from adjustment
Film: Plain film showing L-T scoliosisOnly able to offer relief careDo not try to correct the curve because it isn't going anywhere (in DJD patients)Wolf's law and other models show this to be the case
Special featuresDirectly posterior jetting of annular fibers of disc
Herniation=NP stays connected to AF but pushes out on Annulus FibrosusSequestration=a free floating fragment of NP not attached to Annulus Fibrosus
Hemispherical Spondylosclerosis=half circle of lucency at anterior margin of vertebral bodyShows the body's response to the increase in anterior stressMost commonly seen on lateral view
SI DJDWill have consistent cortical margin vs a tumor which would not
Sacro-Coccygeal jointDJD may show up here as well
DISH=Diffuse Idiopathic SkeletalHyperostosis
May occur at same time as DJD
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Anterolisthesis (DJD)
CT Myelogram Bone window-not showing neuritis!
L-T Scoliosis (DJD)
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What comes up when Google Image Searching Hemispherical Spondylosclerosis?
Dr. Kettner and nothing else! Lecture 6Wednesday, June 04, 20089:17 AM DJD Film: AP Shoulder plain film
Typically onset is predicated by trauma and related irregular contour (thru avascular necrosis or frank damage)Acromio-humeral space is supposed to be non-articular (but supraspinatus lives here)
Point of opposition of rotator cuff group and deltoidPrior avascular necrosis plays an important role in progression (person will feel better prior to actual bone remodeling) Ball and socket joints (especially hip) socket joint surface shapes the 'ball' surfaceIncremental loading is better than jumping up and walking after non load bearing period of recoveryIf person is less than 60 years old and has DJD present then you can't assume 'normal use' was the cause
Film: CT of chest showing Sternoclavicular DJD
May project over lung on plain film
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Film: plain film AP PelvisHip is #1 site of DJD in weight bearing jointsKnee is #2 site of DJD in weight bearing jointsDecreased joint spaceSubchondral sclerosisOsteophytic change occurs after the decreased joint spaceSubchondral cyst is more likely to be seen in the acetabulum than the femoral headFrog leg view may show more osteophytes that are not available on the AP viewOsteophytes may appear as a single hook but because we are only seeing along one angle we may actually be viewing a rounded ridge
Film: Lateral Knee plain filmMay show exaggerated superior pole of patella (owing from increased traction forces)Dystrophic calcification w/in patellar bursa, calcific bursitis (not shown but would be in the superior tendon of the patella)
Film: Tunnel viewMay show wasting of the tibial eminence (which could lead to lateral translation during ambulation)May have bones appearing osteopenic
Film: Sunrise viewHook (osteophyte) may encroach upon cartilage surfacesDystrophic calcific tendonitis may involve calcification of Sharpe's fibers leading to an irregular border of the anterior surface of the patella
DISH=Diffuse Idiopathic Skeletal Hyperostosis (aka Forestier's Disease)If present in the Cervical spine may present w/ difficulty swallowing
Dysphasia occurs in 1/5 of those w/ DISHWhile there is calcification of the ALL it doesn't always alter ROMHypertrophy does not become a problem unless the PLL is involved40% incidence of co-presence of Diabetes Mellitus patients4 continuous segments with smooth and flowing ligamentous hypertrophy and ossification required for DISH diagnosisWill not get a cavitation (adjusting will feel boggy)Predominates T6-11, mid cervicals to CT junction, L3-S1
Film: Cervical Lateral plain filmMajor hypertrophy and calcification of the ALLDisc space remains preservedNo subchondral sclerosis present
Flam shaped SyndesmophyteHas 3 differentials
DISH (Dx by eliminating other disorders)Twin pair=different conditions but look THE SAME on film
Reactive arthritis (Reiter's)Psoriatic arthropathy (must have psoriasis lesions)
Reiter's disease pneumonicCan't see=ConjunctivitisCan 't pee=UrethritisCan't dance w/ me
Osteophyte on calcaneus (lover's heel)Polyarticular arthritisFluid filled pustules on soles of feet
Beuboitis/balanitis=inflammation of glans penis (a classical feature of Reiter's)
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Types of osteophytes/Diff Dx
Osteophyte Features Disorder/Diff Dx
Claw osteophytes Associated w/ disc degeneration DJD
Traction spurs Parallel endplate DJD
Flowing exuberant ossification
Along ALL, PLL DISH
Syndesmophytes Ossification of the annulus fibrosus. Pencil thin Paravertebral ossification (Marginal)
Ankylosing spondylitis, Enteropathic arthritis
Paravertebral ossification
Ossification of connective tissue separated from edge of the vertebral body (C shaped, comma shaped, stuck on, non marginal)
Reiter's Syndrome, Psoriatic Arthropathy
AP Shoulder plain film
CT Sternoclavicular DJD
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AP Pelvis plain film
Lateral Knee plain film
Cervical Lateral plain film
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Lecture 7Monday, June 09, 200810:15 AM
DISHDiff Dx tree (MUCHO IMPORTANO!!!)
Osteophyte?Yes->
Hands?Yes->Erosive Arthritis (Gullwing deformity DIP/PIP)No->DJD. Now claw or traction?
No->Flowing/exuberant->DISHConform to ALL pathway->DISHMaintenance of disc space->DISH Pencil thin marginal->Enteropathic Arthritis (GI issues w/ spinal arthopathies as a secondary component) or Ankylosing Spondylitis
GI Issues?Yes->Enteropathic ArthritisNo->Ankylosing Spondylitis
C-shaped non marginal->Reiter's, psoriatic arthropathy
Skin Lesions (past/present)?Yes->PsoriaticNo->Reiter's
Urethritis, Conjunctivitis, Polyarthritis?Yes->Reiter'sNo->Psoriatic
Flamed shape Syndesmophyte->DISH, Psoriatic, or Reiter'sHLA 8 may be elevated in some DISH patients
Half of DISH patients may have PLL thickening (C and T spine predominate) with some portion having calcification of the PLL also
Discogenic spondylosis (aka spondylosis)=DJD of the spineCheck Sign=visible sign of endplate fracture (looks like V entering into the vertebra from above)
Calcification of ligaments may also show up more in DISH patients
Film: Bone Window CT of C-spineSoft tissue window of CT of C-spineShowing ossification of PLL and the location of the cord is alteredA surgeon should be consulted if the cord is impacted by the PLL hypertrophy
Erosive Osteoarthritis (EOA)=inflammatory variant of DJD involving the IP joints of the handsSometimes thought like an RA presentation (but not)Typically B/L presentationSwelling of the digits (DIP/PIP)Classically a hand disease w/ priority given to the DIP (Distal InterPhalangeal joints)Gullwing Deformity=classic sign of EOA where a down sweep and up sweep down sweep appears across the DIPs1st metacarpal-carpal joint is decreased w/ osteophytic growth (just like DJD) is not needed to confirm diagnosis but will aid as a sign (2nd most common finding)
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PLL HypertrophyPlain Film (DISH)
CT Bone Window (DISH)PLL hypertrophy/ossification
Erosive Osteoarthritis (Gullwing Deformity)
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Lecture 8Wednesday, June 11, 20089:14 AM Table 10.24 diagnostic criteria for RA
Physical1. Morning stiffness2. Pain on motion or tenderness in at least 1 joint3. Soft tissue swelling or joint effusion in at least 1 joint4. Swelling of at least 1 other joint (w/in 3 months)5. Bilateral, symmetrical, and simultaneous joint swelling (except DIP)6. Subcutaneous nodules-boney protuberances (extensor surfaces), justaarticular
Laboratory7. Positive sheep agglutination test (Rh Factor)8. Poor mucin precipitate from synovial fluid (have to aspirate from joint)9. Synovium-at least three of (have to open joint to perform)
a. Marked villous hypertrophyb. Superficial synovial cell proliferationc. Marked inflammatory cell infiltrate fibrin depositiond. Foci of cell necrosis
10. Nodules-granulomas with central necrosis, proliferated fixed cells, peripheral fibrosis, and chronic inflammatory cell infiltrate
11. Typical changes-uniform joint space loss, marginal erosions, etc. (radiographic)Classification
Classic >7 criteria (w/ swelling for > 6 months)Definite >5 criteria (w/ continuous joint symptoms >6 weeks)Probable >3 criteria (w/ continuous joint symptoms) (4-6 weeks)Possible at least 2 of stiffness, pain, welling, nodules, elevated ESR or CRP, or iritis, with joint symptoms for at least 3 weeks
Drawings of joints
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Early pathologic change includes proliferation of pannusBone erosion is a later change (predominately occurring at 'bare area' distal to joint but near the articular cartilage)
Table 10.26 pathologic-radiologic correlation in RA
Pathologic features (physical stuff) Radiologic features (seen on film)
Synovial edema and effusion Periarticular soft tissue swelling
Rheumatoid nodule Subcutaneous soft tissue mass
Cartilage destruction by pannus Uniform loss of joint space
Pannus eroding in the "bare area" Marginal erosion
Intra-osseous pannus and synovial fluid intrusions Subchondral bone cysts
Inflammatory hyperemia Juxta-articular osteoporosis
Periostitis Juxta-articular periosteal new bone (linear)
Fibrous tissue metaplasia Ankylosis
Capsule and ligamentous laxity, tendon rupture Deformity
Film: Left hand showing RA hand with cylastic implant (appears like soft tissue mass)
Implant requires 8-10 hours to applyImplant appears w/ soft tissue contrast and level
Film: B/l hands showing MCP joint and Carpal coalitionCarpal coalition=fusion of the carpal bones (ankylosis)Pencil in cup appearance=head of metacarpal gets thinned and pushes into the phalanx
Film: lateral cervical spine (zoomed to atlantodental interspace)1/5 of all RA patients develop ADI instabilityPannus formation and granulation tissue decreases the integrity of the Cruciate ligamentSafe to x-ray yearly to check progressMay actively translate during flexion/extension views
LHermitte's sign=electric shocks down both arms (think central canal stenosis)If patient has this then do NOT manipulate
Film: AP pelvisBilateral involvement at the acetabulum (symmetric involvement)
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Left femur head representing Protrusio Acetabuli (no teardrop space)Both spaces show no joint spaceDecreased bone density is seen alsoCan't be DJD because it is B/l symmetrical and there are NO osteophytes present
Film: B/l kneesSymmetrical decreased joint space seen on both lateral and medial surfacesReduced cortical space (almost 0) vs medullary portion
Film: lateral knee Arthrogram
Contrast has leaked into Baker's CystBaker's Cyst=represents defect in the capsule allowing herniation of synovial lining beyond its normal chamber (usually contains synovial fluid). Commonly seen w/ RA but may be caused by other conditions
Film: PA chestPleural Interstitial fibrosis-associated finding w/ RA due to it being a systemic condition
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Film: Left hand showing ulnar deviation (RA)
Carpal Coalition (RA)
Film: lateral cervical spine (increased ADI)
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AP Pelvis (RA)
Baker's Cyst (RA)Lateral Knee Plain film
Lecture 9Monday, June 16, 200810:14 AM Juvenile Chronic Arthritis
Formerly Juvenile Rheumatoid ArthritisFilm: Lateral Cervical
Fusion of posterior elements w/ no facet joint seen b/t 2,3,4Anomalous IVFs (shouldn't be seen here)Thin/tall vertebral bodiesADI instability presentDx: sero + JCA
Inflammatory arthritides most common type to produce ankylosisPremature maturation=early closure of the growth platesTypical cutoff age is 14 y/o but may occur as late as 20 y/oFilm: bilateral AP foot view
Dx: Seronegative JCA (Still's disease)Bilateral but not symmetrical
Always do flexion/extension views on JCA patients to document stability/instabilityFilm: AP Pelvis
Joint replacement of hip on right side w/ slipped capitis femoral epiphysis on leftEnlarged obturator foramen bilaterally due to reduced growth inferior and superior pubic rami
Film: 2 views of left handShowing severe ulnar deviationDegradation of carpals is nearly complete w/ no spacing seenDx: seronegative JCAPencil in a cup appearance of metacarpals and proximal end of phalanx
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Ankylosing SpondylitisRailroad track sign=Vertically oriented white lines overlying the pedicle area
Ossification of interpedicle ligaments and ligamentum flavumPencil thin ossification of outer annular fibersGhost joint=No spacing seen of the SI joint (but present on CT)Disuse osteoporosis of vertebral bodies leading to carrying of weight on calcified soft tissuesAssociated w/ HLA-B27 genetic profileFilm: AP Pelvis
Dagger Sign=ossification of interspinous and supraspinatus ligamentSI joints are visualized better but with greater degree of osteoporosis
Progression typicallySITLLumbarCTThoracicCervicals
Equal distribution in men and womenMore prone to fracture (also in unusual locations)
Midvertebral fractureDisc space fracture
Carrot stick fracture=unusual fracture seen in Ankylosing SpondylitisVery common to see dystrophic calcification of ligamentsSyndesmophyte=Calcification of outer annular fibers
Will end up carrying the weight instead of the bodies/posterior elements
Dagger Sign
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AP Pelvis w/ replaced right femoral head (JCA)
Slipped Femoral Capitis Epiphysis (JCA)
Ankylosing Spondylitis
Railroad Track Sign
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Ghost Joint
Lecture 10Wednesday, June 18, 20089:20 AM Ankylosing Spondylitis
Trolley Track Sign=a combination of Railroad sign and Dagger SignStar Sign=pattern made by ossification of soft tissues at top of SI joint in AS#1 cause of death in AS=SuicideDisc ballooning=unrestricted imbibition of NP w/ water increasing its dimension (leading to weakening of cortical margin of vertebral body and deep depressions into the vertebral body possibly both superior and inferior)
May lead to disc calcificationDisc calcification=dystrophic calcification of the disc starting w/ the outer annular fibersIn patients w/ involvement of any sort flexion/extension views are needed to rule in ADI stabilityOrder of progression of AS
Romanus lesion=next step after sacroiliits (then shiny corner sign consisting of focal sclerosis)Shiny corner sign (Romanus lesion)=vertebral body “squaring” with anterior vertebral body corner reactive Osteitis seen on lateral radiographs
Bridging syndesmophyte (calcification of outer annular fibers)Classic presentation
B/l sacroiliitsTL junction40% more problematic inflammatory bowel diseaseHLA B27 from lab testsIf no HLA B27 then check ESR (for Enteropathic Arthritis)
Psoriatic ArthritisPictures of surface lesions of psoriasis10-30% of those with surface lesions will get joint problemsProduces highest percentage of ankylosis in handsFilm: B/l hands
Pencil in cup deformity seen
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DIP joint is affected=Psoriatic ArthritisCarpal coalition presentWill be SeronegativeBilateral and symmetrical=inflammatoryMutilatingDistribution (complete=Ray's Sign)Ray's Sign=complete distribution to all 5 rays (fingers)
Tends to produce normal densityGreater mutilating ability than RA
Greater percentage will have ankylosisIf present in hands (or other small joints) Reiter's must be left outPreservation of bone density (vs RA which does not preserve bone density)Degree of involvement of surface lesions on body does not correlate w/ psoriatic arthropathy100% of people w/ psoriatic arthropathy does have history of skin lesionsMay produce sacroilitis Film: AP Pelvis
Right Femur has moved superior thru softened bonePubic symphysis is bridged along superior portion
Film: Lumbar AP viewStuck on, non-marginal density seen
Radiologic changes in the SI joints w/ Ankylosing spondylitisGeneral
Bilateral, symmetricIliac side is more extensively involvedInitially involves lower 2/3 of joint
Early "sacroiliitis"Articular erosions (Rosary bead)Diminished joint spaceLoss of articular cortex definition (pseudowidening)Patchy reactive sclerosisSubchondral osteoporosis
LateBony ankylosisGeneralized osteoporosis-disappearance of reactive sclerosis"Ghost" joint margin"Star" sign
Reactive Arthritis (formerly Reiter's Syndrome)
Produces pustule like surface lesions on the soles of the feet or palms of the handsWill be different types of lesion than psoriasis
Spine and big jointsUrethritis, conjunctivitis, balanitis, calcaneal spur (also at Achilles' insertion spur)Will have non-osteophyte
No disc problemNon C-shaped but marginal
Film: AP pelvisPubic symphysis narrowed w/ adjacent osteophyte like boneErosion of inferior margin of pubic bones
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Table from Yochum and RoweRadiologic Diff Dx of SI disease
Disease Bilateral symmetric Bilateral asymmetric Uni-lateral
Ankylosing Spondylitis +++ + (early) +(early)
DISH + (upper joint)
Enteropathic sacroilitis +++
Gouty arthritis + + +
Hyperparathyroidism +++
Infection +++
Osteitis Condensans ilii (Pregnant female)
+++ + +
Osteoarthritis (DJD) + +++
Psoriatic spondylitis + +++ ++
Reiter's Syndrome ++ ++ +++
Rheumatoid arthritis + +++
SI Disease Diff Dx
Bilateral SymmetricalAnkylosing Spondylitis
Increasing stiffness w/ agingDagger SignRailroad/Trolley signStar signOsteopenia of vertebral bodiesBridging syndesmophytes
Enteropathic Arthritis
GI disturbances (past/present)Hyperparathyroidism
Low levels of Parathormone in circulationOsteopenia
Osteitis Condensans IliiPost-multi parity female
Bilateral AsymmetricalPsoriatic Arthritis
Focal/global skin lesions (past/present)Unilateral
DJDOsteophytesSubchondral sclerosisSubchondral cystsAsymmetrical (across joint) space lossAsymmetrical distributionSero -
Reiter'sConjunctivitisUrethritisCalcaneal spur
Often asymptomaticSero -
RheumatoidSero +Likely hand involvement Uniform joint space lossMorning stiffnessPannus formationLots of soft tissue swelling
InfectionInfective agent within joint capsule
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Ankylosing spondylitisDagger Sign
Star Sign
Shiny Corner Sign
B/L hand view w/ Psoriatic Arthritis
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Reactive Arthritis
Lecture 11Monday, June 23, 200810:18 AMTable 10.53 Diff Dx of Psoriatic arthritis
Feature Psoriatic Arthritis Reiter's Syndrome Rheumatoid Arthritis Ankylosing Spondylitis
Distribution
Upper extremity hand +++DIP/PIP
--
+++MCP/Wrist
+
Lower extremity +++ +++ +++ -
SI ++ ++ + +++
B/l ++ ++ (asymmetric) + +++
U/l ++ +++ +++ +
Spine ++ + +++ (cervical) +++
Key Signs
Osteoporosis + +++ +++
Joint space +++ (widening) + (narrowing) +++ (narrowing) ++ (narrowing)
Ankylosis ++ - + +++
Periostitis +++ (fluffy) +++ (fluffy) + (linear) +++ (fluffy)
Tuft resorption +++ - - -
Soft tissue swelling ++ ++ +++ +
Laboratory
ESR + ++ +++ +++
RA Factor - +++ -
HLA-B27 60% 75% 8% (normal) 90%
ScaleRare -Occurs +
More common++Very common +++
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Dystrophic calcificationCalcific tendonitis/HADD (Hydroxy-Apatite Deposition Disease)
Film: AP and oblique foot (unilateral)Concretion of Peroneus longus tendon (dystrophic calcification)Will occur due to change in pH and may lead to spontaneous ruptureLikely suffered several inversion injuriesLooks similar to Os Peronei but won't be palpableComposed of HADTx: ultrasound
Film: AP ShoulderShowing calcific tendonitis of the supraspinatus where it attaches to the greater tubercle of the humerusChanges in pH due to blood-flow changes w/in the bursa cause precipitation to occur
Metabolic arthritide Gout
Tophi=uric acid crystal accumulation on the pinna of the earSodium monourate=uric acid crystalsBig toe is major spot where Gout shows upBone changes created due to pannus formation began under deposition of uric acid crystalsOverhang sign=overhanging of one bone upon an adjacent boneTypically not seen on radiographs now due to early treatment
Calcific Tendonitis (Shoulder)
Tophi of ear (Gout)
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Overhang sign
Lecture 12Wednesday, June 25, 20089:18 AM Continuing metabolic arthritide
GoutMetabolic arthritideAberration of purine pathway->uremia->(Uric acid crystal deposition)Transient processDeposition occurs in smaller vessels w/ slower flowBreak in lesion=classic radiographic sign of Gout producing Overhang SignAvascular necrosis due to blood vessel impactionNot a tremendous risk to the kidneysFilm: B/l foot AP film
Overhang sign presentMucho soft tissue swelling (may make you think infection)
Film: B/l hand AP filmLots of small depositions in the phalangesDystrophic soft tissue calcificationTophaceous Gout=metabolic arthritic disorder producing soft tissue calcification after uric acid deposition
No organizationFilm: Lateral knee
Lucency seen in proximal tibial shaftInitial Diff Dx: cyst, enchondroma, Giant Cell tumorCT of same patient shows very sclerotic margin (slow onset)Biopsy shows uric acid crystalsDx: Intraosseous Gout
CPPD (Calcium PyroPhosphate Dihydrate Deposition)Will likely become the poster-child for metabolic disorders later Joint space is NOT blackSome Calcium pyrophosphate deposition in the joint spaceFilm: AP knee
Lines or triangles seen b/t articular cartilagesFilm: AP shoulder
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What appears to be thickened cortical margin but upon closer inspection is not connected to cortical margin
Homogentisic acid (aka: Alkaptonuria/ochronosis)Dermatology Slide: Ear
Darkening skin in superior pinna of earDarkened skin on cheekBlackening due to oxidized homogentisic acid
Pt is missing enzyme: homogentisic acid oxidaseTakes long time to develop in the body (genetic disorder)Onset around age 30Lab finding: urine will turn black if left exposed to airNo osteophytes normal corticesNo bony hypertrophy, no subchondral sclerosisFilm: AP lumbar
Multi-level degeneration and major sclerosis (S1-L4)DJD in wrong age and wrong distribution
Film: Lateral ThoracicNormal cortices but calcification of disc spaces
HADD (Calcific tendonitis)Film: AP and oblique foot (unilateral)
Concretion of Peroneus longus tendon Dystrophic calcification=occurs due to change in pH and may lead to spontaneous ruptureLikely suffered several inversion injuriesLooks similar to Os Peronei but won't be palpableComposed of HADD (Hydroxy-Apatite Deposition Disease)Tx: ultrasound
Film: AP ShoulderShowing calcific tendonitis of the supraspinatus where it attaches to the greater tubercle of the humerusChanges in pH due to blood-flow changes w/in the bursa
OCI (Osteitis Condensans Ilii)
10:1 Women: menBrought on by multiple full term pregnanciesBright triangle of sclerosis along iliac margin of SI jointFilm: AP Pelvis
Classic bright triangle of sclerosis in ilii Hypertrophic Pulmonary OsteoArthropathy (HPOA)
Looking at the trabecular bone, then cortico-trabecular interaction, cortical bone then we see some of the periosteal tissue (periosteal reaction)Typically due to either reduction of lung function or metastatic bone disease Solid periosteal reaction is presentIf no lung disease present HOA (Hypertrophic OsteoArthropathy)is presentClubbing will be present
MiscScleroderma
CREST SyndromeCalcinosis (calcium deposits, usually on fingers)Raynaud phenomenon (Red, White, Blue fingers)Esophageal dysmotility (inability to swallow)Sclerodactyly (tapering deformity of bones, seen on X-ray)Telangiectasia (red spots seen on fingers/mouth)
Difficulty protruding tongue
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Difficulty opening mouthTruncated=retraction of skin at fingertipsReduction of blood flow to and from the distal extremities due to aberrant connective tissue depositionAcroosteolysis=consumption of distal portion bones w/in extremities
Systemic Lupus Erythematosus (SLE)Changes soft tissues not boneSmall joint diseaseAppears like RA but pt will be able to flatten hand to film (Reversible Subluxation)
Break in=something breaking into the bone (pannus). Will carry a solid cortical marginOsteopoikilosis=polka dots w/in boneSynoviochondrometaplasia=metaplasia of synovial cells into cartilage (and later bone) within the joint capsule but outside the cortical bone
Typically affects only 1 joint at a timeAppears as polka dots (joint mice) outside the cortical bone and within the synovial capsuleIntracapsular and extra corticalJoint will 'lock' (due to 'joint mice)Tunnel view is best to view joint miceLoose chondral bodies w/in joint at to predispose to DJDPressure erosion of nearby bones may occur (may produce Apple Core Deformity)
Dystrophic calcification of the glenoid labrumPigmented Villonodular Synovitis=villous tissue hypertrophies to produce synovial fluid they attract hemosiderin
Apple Core Deformity=pressure erosion of bone Break In Lesion (Gout)
Tophaceous Gout
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CPPD AP Knee
Alkaptonuria
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HADD (Calcific Tendonitis)
Osteitis Condensans Ilii
Hypertrophic Pulmonary OsteoArthropathy
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Scleroderma
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Systemic Lupus Erythematous (SLE)
Osteopoikilosis
Synoviochondrometaplasia
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Pigmented Villonodular Synovitis
Lecture 13Monday, June 30, 200810:17 AM Arthritides of the Axial and Appendicular SkeletonDr. Bonic DC RT® 25 cases w/ arthritides then normal w/ abnormal Case 1
DISHDish space/Z joint preservedExuberant hyperostosis on 4 continuous levelsPLL may ossify
Case 2
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RhAADI enlarged (3 mm+)Disruption of spinolaminar lineOsteopeniaB/l symmetricalTypically shows
Uniform joint space narrowingMarginal erosionsDeformitiesAtlantodental instabilityProtrusio acetabuliOsteopeniaRotator cuff tears
Case 3DJD
IVD narrowingOsteophytesUncovertebral and Z joint arthrosis/sclerosis (may narrow IVF)
Case 4JRA
Atlantodental instabilityApophyseal ankylosisHypoplasia of vertebral bodies and discsOsteopenia
Case 5Ossification of PLL (DISH)
May compromise spinal canalCase 6
Ankylosing SpondylitisThin, marginal syndesmophyteAnkylosis of apophyseal jointsDecreased lordosis and marked anterior head carriage often seenADI instability likelyCarrot stick pathologic fracturesSpinous process erosion
Case 7Infectious discitis
Widened retropharyngeal and retrotracheal soft tissuesCortical destructionIVD narrowing
Case 8Ankylosing spondylitis
Thin, marginal syndesmophytes'Bamboo spine''Trolley track spine'IVD calcificationDagger sign=interspinous calcification
Case 9Reiter's
Non-marginal syndesmophytesCan't pee, can't see, can't climb a treePolyarthritis
Lover's heel
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Non marginal syndesmophytesB/l sacroiliitis
UrethritisConjunctivitis
Case 10Apophyseal Joint Arthrosis
Hypertrophy and arthrosis of Z-jointsMay change in pedicle-facet angle leading to non Lytic/fracture Spondylolisthesis
Case 11Discogenic spondylosis (DJD)
IVD narrowingOsteophytosisDiscovaccum phenomenon
Case 12Villonodular
B/l sacroiliitisMay fuse SI jointsWill then ascend into lumbar spine
Case 13Psoriatic arthritis
Psoriatic skin lesionsNon-symmetricalErosive changes, widening of SICommon=SI, hands (DIP), feet (DIP), spine
Case 14Rheumatoid arthritis
Carpal fusionB/l symmetricalMCP deviation to ulnar sideSwan neck deformity (Boutonniere deformity)=flexion deformity of PIP, extension deformity of DIP
Marginal erosionCase 15
Psoriatic arthritisMCP intact (rules out RhA)Fusiform swellingPredominately affects DIPPencil in cup deformity
Case 16
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GoutSodium monourate (uric acid) crystal depositionMetabolicMarginal erosions, IntraosseousOverhang signUnilateralDistribution is definitiveTophi, bone erosions (long standing only), normal bone density seen
Case 17Scleroderma
Soft tissue changesTapered conical fingertips, retraction of tip (truncation), soft tissue calcification
Resorption of distal tufts (Acroosteolysis)Normal joints
Case 18Synoviochondrometaplasia
Benign arthropathy3-5th decadeCalcific loose bodies outside joint capsule (joint mice)May produce erosions on the bone
Case 19Neuropathic Arthropathy (Joint Disease)
6 D's "Bens lot", "De, De, De, Dis, Dis, Dis"DebrisDensityDestructionDislocationDisorganizationDistension
Case 20Pigmented villonodular synovitis
Usually affects 1 jointEffusion'Apple core deformity' secondary to extrinsic erosions
Case 21HADD (calcific bursitis/tendonitis)
Calcification of tendons, bursas, capsulesHydroxyAppatite Deposition diseaseShoulder, hip, spine
Case 22CPPD
Calcium PyroPhosphate Dihydrate depositionHot tender swollen jointsKnee, wristPyrophosphate arthropathy may be seen
Atypical locationSubchondral cystsDestruction changes in listSlac risk (scapholunate advance collapse)
Case 23Juvenile Chronic Arthritis (formerly Juvenile Rheumatoid Arthritis)
Hyperemia seen
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Accelerated growth in epiphysis leads to ballooningOsteopenia seenSoft tissue swellingUniformed joint space narrowingAnkylosis possibleLinear Periostitis
Case 24Systemic Lupus Erythematosus
Deforming arthropathy w/out permanent changes (Reversible Subluxation) Swann neck deformityAffects many systemRash, Arthralgia
Case 25Primary OsteoArthritis
Peripheral erosions of distal phalanx 'Gull wing Sign'OsteophytosisNon-uniform joint space lossAnkylosisSubchondral sclerosis
Lecture 14Wednesday, July 02, 20089:16 AM Neurotrophic joint disease
Not only do we have the kind we normally think about but there is finer proprioception within joints (keeping the cartilage from banging together)Damage results from loss of proprioception functionMay be associated w/ diabetic neuropathyHypertrophic joint disease
Characterized by 6 Ds/(BNSLOT)Debris (from destruction)Density (subchondral intensity increase)DestructionDislocation (or feels like it/to much motion)DisorganizationDistension
Occurs in weight bearing jointsCase: 52 year old woman w/ diabetic neuropathy
Calcaneus is pretty destroyedTalus is almost totally missingThis patient walked in, felt the joint was unstable
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Atrophic Joint DiseaseSmall non-weight bearing jointsSurgically amputed appearance or Candy lick appearanceCandy lick appearance=smooth cortical bone and worn down to a fine point
3 causesDiabetes MellitusTabes dorsalis=a slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brainSyringomyelia
Typically occurs in the shoulderC-spine surgeryDue to formation of Syrinx w/in cordSyrinx=CSF cyst w/in spinal cord
Enteropathic ArthritisActs as a complication to Chron's or Ulcerative ColitisRadiographic twin for Ankylosing Spondylitis
Distinguish by history (will have GI issues) and HLA B27 (will not be present in EA but will be in AS)Predict as male
Atrophic Neurotrophic Joint Disease
Syrinx/Syringomyelia
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Enteropathic Arthritis
Lecture 15Monday, July 07, 200810:15 AM Video of Dr. Gross (guy w/ Ankylosing Spondylitis)
Defect on 6th chromosome creating an abnormal charge potential in collagen strandsThis happens all over the bodySigns of collage disruption=idiopathic sore throats, recurrent bladder infections, eye irritationOnset of signs occur in the twentiesHLA-B27 is positive only after pubertyGait=shuffle w/ arms extended posteriorly as balance/pain reliefPrimary causes of death
Suicide
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Congestive heart failureHypertension->strokeFracture, dislocation of C/S following MVARenal failure typically liked to medical complicationsAcute liver failureSecondary leukemia associated w/ radiation therapySurgical complications
Traditional medical treatmentsNSAIDsMuscle relaxantsAnti-depressants-you still feel the pain but don't give a damnBlood thinnersPain killersJoint replacements as indicated
Alternative therapy optionsRegularly scheduled chiropractic careNutritional supportStrength and mobility exercises (pain can't hit a moving target)Emotional support groups and professional counselingLifestyle assistance devices and optionsMassage therapy for pain control and flexibility
Dr. Stan's Nutritional programAscorbic acid: 10-15 grams/day (gradual delivery)Beta glucans: yeast derived immune support 600 mg dailyA high quality multivitamin/multimineral baseHyaluronic acid: 150 mg natural anti-inflammatoryExtremely limited refined carbohydrates-raw fruits and vegetables preferred-avoidance of processed foodsModerately limited meat and animal products1-2 gallons of water per day (80% compliance is acceptable)Fiber, fiber, more fiber
Dr. Stan's Lifestyle ModificationsDressing successfully (simple modifications to make getting dressed a little easierGadgets galore (walking sticks, arm extenders)
Make list of things that you would do if you didn't have AS (then show them how they can do these things)
Exercise for the unique physique (swimming and aerobic workouts)Not accepting limitations (find out goals and help them accomplish those goals)Staying motivated (realize that AS isn't the end of the world)
Other problems to considerNumber of joints replacedAge of onset (often mis-diagnosed)The support systemThe level of progressionThe emotional supportOther health complicationsComplications from medications
ListsSunday, July 06, 2008
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3:55 PM Degenerative Arthritides
DJDErosive ArthritisDISHOPLLNeurotrophic ArthropathySynoviochondrometaplasia
InflammatoryRheumatoid ArthritisJuvenile Chronic Arthritis (Juvenile Rheumatoid Arthritis)Reactive Arthritis (Reiter's)Ankylosing Spondylitis
PsoriaticEnteropathic ArthritisSystemic Lupus ErythematosusScleroderma Osteitis Condensans IliiHypertrophic Osteoarthropathy
MetabolicGoutCPPDDHADDOchronosisPigmented Villonodular Synovitis