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OSTEOARTHRITIS

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ishanSINHA on Oct 05, 2009 Says :

its a nice presentation

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want this

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nice

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news

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nicely elaborated exercises protocol to be incorporated

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Show Notes

Slide 1 :

OSTEOARTHRITIS Dr. Gaál János Department of Rheumatology,Kenézy Gyula Hospital

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2 OSTEOARTHRITIS (ARTHROSIS) Definition: the gradual, progressive impairment of all structures of the joint with the consequential pain and loss of function Important: heterogenous process Prevalencia: high, 30% of adult population, (above 60 years radiological involvement: 90%!) Incidence: 88 (hip)- 240 (knee)- 300 (hand) patients/year/100 000 Significance: most prevalent disease, most common cause of disablement, frequency of NSAID prescription!

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3 The underlying cause: probably multifactorial passing into man, (erected gait, working with hands) (knees, I CMC) Longer life span Genetic background (2q, VDR, ER, IGF1, IL1ß, COL2A1) Factors rising the impairment: mechanical: obesity,congenital abnormality, macro- microinjury, overuse, prior arthritis,aseptic bone necrosis metabolic: disturbances of collagen synthesis, haemochromatosis, acromegalia, ochronosis etc.tb. immunological: autoimmune inflammation THE CAUSESOF OA

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4 Alterations in OA cartilage Metabolic changes Il1-TNF? induced MMP activity, serin and thiol proteases Decreased of TIMP, PAI activity Chondrocyte proliferation, hyperploidity, hyperplasia, hypermetabolism, increased apoptózis Biochemical changes Decreased proteoglycane concentration Inordinate collagen network Immature intercellular matrix Fat deposition around the chondrocytes Biomechanical changes Decreased resistance against compression Rough surface, friction Pathological changes Fibrillations, fissurae, eburneation Deposition ofcalcium containing crystals Widening os osteo-chondral border

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5 Immunological alterations in OA cartilage Chondrocyte activation (MHC-II, CD 80, CD86 expression), antigen presentation Autoantigen release Cytokine (IL-6, 17, 18, LIF) and chemokine (IL-8, RANTES) production Superinduction of COX-2, NOS genes

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6 Alterations is OA joint Subchondralis microfractures-reparative sclerosis Cyst formation, reactive bone formation Periarticular and intraarticular calcium deposition (CPPD, BCP) Periarticular muscle atropy Periarticular inflammation

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7 Immunological alterations in OA joint Synovialis hypertrophy, lymphocytic infiltration Participation of cellular immunity: restricted clonal synovial expansion of CD3 and ? IFN positive (Th1) cells Participation of humoral immunity: deposition of autoantibodies (against chondrocyte membrane, cartilage link protein, aggreane, YKL-39, osteopontin, TPI /triose phosphat isomerase/), immuncomplex deposition Endothel activation: E-selectin (CD62E) Angiogenesis: endothel proliferation, macrphage infiltration,VEGF superinduction in synoviocytes Detritus synovitis?

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8 Genetic predisposition Obesity Aging Local biochemical factors Occupational or sport stress Increased matrix degradation, Metalloproteáz ?, TIMP?, IL1?, NO,PG, TNF? ? Decreased matrix Synthesis ßFGF,IGF-1,TGF-? ? Subchondral bone alterations Increased bone turnover Subchondral sclerosis Osteophyte formation OSTEOARTHRITIS Pathogenesis Imflammation

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9 RISK FACTORS OF OA Trauma Repeated stress, overload, certain sports Obesity Age Genetic factors (e.g.kollagen II gen mutions, COL2A1) Gender (female) Congenital abnormalities Prior arthritides Metabolic and endocrin disorders

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10 CLASSIFICATION Primer Localised Generalised Erosive (PIP,DIP, 15%-RA kriteria) Secunder Posttraumatic Inherited connective tissue abnormality ( Marfan, Ehlers-Danlos) Vitamin, Se, I deficiency (Se-I?Kashin-Beck) Congenital abnormality (dysplastic hip, epiphyseal dysplasia) Metabolic disease (ochronosis, hemochromatosis, Wilson disease Gaucher) Krystal arthropathy (urat, CPPD, hydroxyapatit) Endocrine disorders (diabetes, hyperthyreosis, hypothyreosis hyperparathyresis, acomegalia) Neurogen arthropathy Other locomotor disease (RA, Paget, aseptic necrosis)

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11 Complaints Pain at start after a long-lasting rest Pain in a joint during or after use (from mildly inconvenient to disabling) Discomfort in a joint when the weather changes Swelling and stiffness in a joint, particularly after using it Bony knobs (nodes) on the finger joints may create a gnarled appearance. Back and neck pain and stiffness from slow deterioration of discs between the bones of the spine.

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12 CLINICAL SYMPTOMS, SIGNS Articular pain (complex origin) Morning Stiffness Functional impairment Unstability Decreased range of motion Decreased muscle strenght Crepitation, crackling Swelling, deformity Alteration of axis

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18 DIAGNOSIS Mechanical articular pain (MS, pain at starting) + Impairment of function (instability, decreased range of motion, decreased muscle strenght, deformity)

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19 Imaging procedures Just to complete the clinical dg Convencional Rtg (narrowing of the articular space, sclerosis, osteophytes, cysta formation) CT (differential dg) MR (small intervertabral joints) Scintigraphy (Paget, tumor, met, femur head necrosis) UH (synovitis, Baker cyst, ligament ingury) Arthroscopy (direct vizualisation, sampling, th)

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20 LABORATORY METHODS Inflamatory activity (ESR, CRP) Synovial fluid Biochemical markers Cartilage: urine pirridinoline crosslinks, hydroxyprolin Bone: AP, osteocalcin, vizelet deoxypirrdinoline crosslinks

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21 Therapy

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22 Pain killers (analgetics) Nonsteroidal anti-inflammatory drugs (NSAIDs) (traditional and COX 2 selective) These both relieve pain and reduce inflammation. Topical pain relievers (creams, gels, ointments and sprays) temporarily relieve arthritis pain and reduce inflammation in joints close to the surface of the skin most frequently used: methyl salicylate, menthol and camphor; or capsaicin from the seeds of hot chili peppers Antidepressants. Corticosteroids (intraartucular) Viscosupplementation:Hyaluronate (Hyalgan) pain relief is usually achieved more slowly with shots than with corticosteroids, but it lasts longer. Joint replacement: hip, knee, shoulder, elbow. Other surgical procedures to remove loose pieces of bone or cartilage that may cause pain or locked joints reposition the bones Correction of deformities or fuse bones to increase stability and reduce pain Treatment options

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23 Psycho-social treatment Analgetics NSAID ointments NSAID minor dose NSAID th. Surgery Intraartikular steroid, chondroprotection Physiotherapy Therapeutic pyramid of OA

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24 Non drug treatment Pszicho-social treatment Information, guiding, education Lifestyle and dietetic changes Psycological aid Patient clubs Weight loss Patient contact Medical aids (braces, wedged insoles, sticks) Other treatment modalities Physiotherapy Surgery

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25 Physiotherapy Improves: Aerob capacity Muscle strenght Coordination of movement Dynamics of the gait Quality of life Most important:special exercise Decreases the pain

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26 Physiotherapy II. Thermotherapy Kryotherapy Mechanotherapy Low frequency elektrotherapy Interference Magnetotherapy Laser? Manualtherapy? Akupunkture?

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27 Advices for the patients Exercise regularly. Control weight. Eat a healthy diet: vegetables, whole grains and fruits Avoid actions that strain finger joints Spread the weight of an object over several joints. Take breaks to relax, and stretch regularly. Maintain good posture. Use your strongest muscles and favor large joints. Apply heat (15-minute hot shower or bath, hot pack, an electric heating pad) Apply cold for occasional flare-ups Wear comfortable, cushioned shoes that support your weight. Practice relaxation (hypnosis, guided imagery etc.). Keep a positive attitude. Studies show that people who take control of their treatment and actively manage their arthritis have less pain and function better. Use braces, stick or special tools that help you have an active, independent life. Take medications as recommended.

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LOW BACK PAIN

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29 OA OF THE SPINE disc degeneration disc herniation, spondylolisthesis lumbago, lumboischialgia cervicobrachialgia dorsalgia small joint OA osteophyte formation (spondylosis) spinal stenosis spinal claudication

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30 Causes of low back pain Mechanic: disc degeneration, herniation, spondylarthrosis, spinalis stenosis, spondylolisthesis Inflammation: spondylarthopathies, sacroileitis, infektive process Malignant process: primer tumor, metastasis, myeloma multiplex Vertebral fracture Generalised metabolic bone disease: osteoporosis, osteomalatia, hyperparathyreosis, Paget disease Retroperitoneal and perineal tumor Referred pain (renal stone, aortic anaeurism, pancreatic tumor vagy retroperitoneal process) Psychogen origin

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31 Clinical syndromes Vertebral symptoms: spinal pain, muscle spasm, antalgic gait, tenderness Radicular symptoms: pain, paraesthesia, numbness, streching symptomps, motor weakness, decreased reflexes, aggravated with increased intraabdominal pressure

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32 Diagnosis Basis first physical exam is enough (tendency for spontaneus impovement) X-ray: not necessary at first presentation Indications: incapacitating pain or progressive symptoms, known cancer disease,spinal injury CT, MRI, scintigraphy: for excluding other,serious disease, before the planned operation Laboratory: to exclude infection, tumor, inflamation, metabolikus disease (ESR, CBC, urine, AP, Ca, P, hepatic function, se. elektrophoresis)

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33 Indications for urgent diagnostic/therapeutic interventions Fever,weight loss, ESR , pain at rest: infection, tumor, vertebral fracture First appaerance over 50 years: tumor, vertebral fracture Muscle weakness, bladder, bowel function disturbances: herniation, cauda syndrome First appearance under 30 years: sacroileitis, congenital spinal abnormality Antecendent cancer disease Concomitant peripheral arthritis, enthesitis: SNSA

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34 Treatment of vertebrogenous low back pain Bed rest: max.4 days! Pain relief: analgesisc, NSAID, tramadol, corticosteroid treatment for<1 week,musclerelaxants, local steroid-lidocain injections, antidepressants, TENS, PENS Physiotherapy: ointments, special manipulations Mobilisation as early as possible: special exercises, after the acute phase elektro-mechano-balneo treatment Operation: cauda syndrome, progressive paresis, unsuccessful konservative treatment for 3 months Patient education, „back school”-strenghtening of paravertebral muscles Rehabilitation: exercise at home (day to day), psychotherapy, back to the original work!!!

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Infektive (bacterial) arthritis

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36 Definition Arthritis, caused by infective agent (bacteria) This agent detectable from the synovial fluid/membrane

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37 Significance Extremely destructive Rapid course without treatment Mortality is relatively high (5-15%)

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38 Pathophysiology Characteristics of synovial membrane Hypervascularised No basal membrane Relatively closed space Bacteria can easly adhere and colonise Spreeding Hematogenous (90-95%) Direct inoculation (operation, „thorn synovitis”) Continous spreeding from adjacent bone/soft tissue

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39 How can get the bacteria into the joint?

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40 Clinical symptoms Acutely painful, swollen joint(s) (10-20% polyarticular) Decreasing range of motion (active and passive) Systemic symptoms (fever, weakness, shaking chill at bacteriaemia) Distribution of affected joints: (knee 55%? hip 11% ?schoulder 8% ?wrist 7% ?elbow 6% ?others 5%)

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43 Diagnosis Most important: arthrocenthesis blindly (if needed fluoro- scopy/CT guided) or surgical method to get synovial fuid Examinations: LDH, glucose, WBC, TP, crystal analysis, culture (aerob, anaerob, Neisseria or Hemophilus suspicion: chocolate agar), Gram stain, Blood culture: positive in 50% Orientating findings: high LDH, TP, WBC, low, glucose content

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45 Imaging procedures Early and late X-ray (joint fluid-aricular space dilation-increased soft tissue shade- periarticular osteoporosis-articular space narrowing-erosions) Special findings (gas formation, epiphyseal destruction, osteolysis, metaphyseal periostitis) CT, MRI (hip, shoulder, sternoclavicular, SI joint) 3 phase bone scan (streaming in, blood pool, late phase), TC99m HMPAO leukocyte scan, Tc99m anti-granulocyte scan

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48 Definitive dg: bacteria, using Gram stain/culture from synovial fluid/membrane

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49 Predisposig factors Immuncompromised patient (steroid, immunsuppressive th.) Alcoholism Uraemia Diabetes mellitus Cancer Combustion Sickle cell anaemia (Salmonella) HIV infection (S. Aureus, Salmonella) I.v. drug users (recurrent bacteriaemia): 75 % MRSA, 11% Pseudomonas, Repeated arthrocenthesis, intraarticular steroid,arthroscopy

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50 Predisposig factors Associated arthritis RA: 0,3-3% incidency, long standing, erosive, seropositive disease, steroid treatment, Staphylococcus 75%, Streptococcus 15%, Gram negatives 7-8% Crystal arthropathies: wide pathogen spectrum Severe osteoarthritis Neurogen arthropathy Hemarthrosis (hemophylia, bleeding tendency) SLE: Salmonella (carrier status), Neisseria, Proteus (functional hyposplenia)

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51 Prosthetic joint infections Early (within 3 months) infection: fever,pain, swelling Risk factors: long lasting surgery, number of personals in theatre, inexperienced surgeon, advanced age, RA/systemic immune disorder, perioperative non articular sources of infection pathogens: S. aureus, S. epidermidis Late infection (after 1 year): long course, smouldering but increasing pain Risk factors: RA, infective sources, old type of prothesis, age of prothesis, dislocation Important: to distinguish the septic and aseptic dislocation: X-ray, ESR, CRP, scintigraphy (Tc99m HMPAO leukocyta, anti granulocyte, polyclonal immunglobuline scintigraphy, microsphere, nanocolloid), aspiration, culture Profilaxis: preoperative screening of occult infections, fast eradication, decreasing of immunesuppression, antibiotic prevention of high risk or contaminated patient, antibiotic-impregnated cement

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52 Bacterial spectrum

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53 Therapeutic algoritm Suspicion Punction Non purulent Purulent Gram stain: bacteria Gram stain: no bacteria Time for vaiting for the culture Final antibiotic due to sensitivity Gram - aminogl.+ penicillin or 3. gen.cephalosp. Gram + Immuncompromised patient No Methicillin or ciprofloxacin Yes Vancomycin or rifampicin

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54 Outcome Mortality: 5-15% Chronic joint impairment:25-60% Factors affecting the final outcome: Duration of the infection Virulence of the pathogen The diseased joint (hip!) The patient’s age Co-morbid states Host defenses

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55 Disseminated Gonococcal infection

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56 Disseminated Gonococcal infection Pathogen: Neisseria gonorrhoeae Significance: most common in adults, exellent liability to healing Tipical clinical picture: polyarthritis (25-50% purulent) tenosynovitis, dermatitis (maculo-papules, vesicules, pustules) Latent period: 1-60 nap Urogenital symptoms: 25% Dg: culture (blood 25-50%, punctatum 25-70%, urogenital 80-90% positivity), PCR (tipical clinical picture+negative culture) Differential Dg: other bakterial arthritis, endocarditis, Reiter sy, hepatitis, reumatic fever, Lyme, viral arthritis Th: 4x500 mg ampicillin p.o. v. 1g cephtriaxon v. 2g erythromycin v. 2g ciprofloxacin v. spectonomycin 2x2g for 1 week

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57 Intervertebral space infections Commonest localisation: lower Th, L spine Spreeding: hematogenous in child, after operation or discography in adult Clinical picture: increasing pain after surgery spinal pain, muscle spasm, systemic symptoms Dg: ESR, WBC, X-ray (space narrowing, erosions later),MRI, scintigraphy (Tc99m, leukocyte, Ga, Inflammon, anti granulocyte), blood culture, needle aspiration/sampling by surgery: culture!!! Pathogens: S. aureus, S. epidermidis

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