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35 Cards in this Set
- Front
- Back
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Approach to monoarthritis
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Inflammatory vs non-inflammatory:
Non-inflammatory = osteoarthritis Inflammatory = Infection, crystals, blood, other Infection = Staph, Gonococcal, Fungal, other Crystal = gout, pseudogout Blood = trauma, coagulopathy |
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Septic Arthritis: Causes
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Hematogenous spread of:
Gram-positive cocci (75-80%) Gram-negative bacilli (15-20%) S. aureus is most common |
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Septic Arthritis: Risk Factors
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Recent infection
Portal of entry Prosthetic joint Diseased/deformed joint Immunocompromised Elderly *Sexual activity (gonococcal) |
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Septic Arthritis: Presentation
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Acute pain and swelling
Knee and HIp |
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Septic Arthritis: forms of gonococcal infection
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1. Typical septic arthritis
2. Disseminated gonoccocal infection (DGI) |
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Signs of DGI
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Migratory arthritis + skin lesions + tenosynovitis
Positive cultures at sites other than blood and synovial fluid |
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Septic Arthritis: Synovial fluid characteristics
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Turbid/purulent
Low viscosity WBC > 2000 with high percentage of pmn cells |
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Septic Arthritis: Blood work findings
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Elevated WBC
Elevated ESR |
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Septic Arthritis: Xray findings
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Synovial effusion and soft tissue swelling
No us except as baseline image |
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Septic Arthritis: Management
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Synovial fluid cultures for GS and culture
If turbid and purulent then empiric antibiotics Refine antibiotic choice based on culture results Daily needle drainage Early physio |
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Septic Arthritis: Antibiotic choices
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Gram +ve cocci: vancomycin
Gram -ve bacilli: 3rd generation cephalosporin Gonococcal: ceftriaxone * IV 1-2wks then oral 2-4wks |
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Septic Arthritis: Prognostic factors
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Old age
Preexisting joint disease Presence of prosthetic joint |
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Crystal induced arthritis: types of crystals
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monosodium urate: gout
calcium pyrophosphat (CPPD): pseudogout Calcium hydroxyapatite |
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3 C's of synovial fluid analysis post arthrocentesis
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Culture
Cell Count Crystals |
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Crystal induced arthritis: pathogenesis
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Crystals deposit in synovial tissue, cartilage and periarticular structures
Crystals promote acute inflammatory attacks Destructive changes if becomes chronic |
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Gout: epidemiology
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Men >40, Women post-menopausal
Joints: 1st MTP, ankle, foot |
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Gout: Uric acid regulation
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Dietary intake: red meat, fish, beer will increase production
Synthesis: critical illnesses, ethanol, etc. will increase production Excretion: renal failure, metabolic syndrome, diuretics will decrease excretion |
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Tophaceous deposits
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Deposits of urate crystals seen in chronic untreated gout
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Crystal induced arthritis: diagnosis
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1. Presence of acutely inflammed joint
2. Presence of crystals in synovial fluid |
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Crystal induced arthritis: Role of Xrays
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Indicate chronic gout disease
Cannot see acute gout |
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Pseudogout (calcium pyrophosphate dihydrate deposition disease): pathogenesis
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Release of crystals from cartilage into joint leads to inflammation and pain
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Pseudogout (calcium pyrophosphate dihydrate deposition disease): epidemiology
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Age>60
Joints: wrist and knee |
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Pseudogout (calcium pyrophosphate dihydrate deposition disease): role of xrays
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May indicate CPPD
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Crystal induced arthritis: hydroxyapatite epidemiology
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Young
Joints: shoulder, hip, 1st toe |
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Crystal induced arthritis: Management of acute attacks
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Rest, ice analgesia
NSAIDS Colchicine corticosteroid injection |
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NSAIDS: mechanisms of action
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anti-inflammatory
analgesic antipyretic antiplatelet |
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NSAIDS: adverse effects
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Bleeding
Renal dysfunction Salt and water retention (hypertension, heart failure) Dyspepsia/GI ulceration Inhibition of uterine motility Allergic reactions |
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NSAIDS: prevention of grastropathy
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Try acetominophen first
Switch to Cox-2 specific PPI Prostaglandin E1 analogue |
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Colchicine: mechanism of action
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disrupts chemotaxis and phagocytosis of urate crystals to reduce inflammation
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Colchicine: side effects
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Early: diarrhea and abdo pain
Severe: bone marrow suppression, multi-organ failure |
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Crystal induced arthritis: Prevention
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Dietary modification
Avoid drugs that increase uric acid (diuretics, ASA, cyclosporine, ethanol) Urate lowering therapy (Urocosurics, allopurinol) |
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Urate lowering therapy
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Uricosurics: increase excretion of uric acid
Xanthine oxidase inhibitors (allopurinol): decrease production of uric acid |
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Allopurinol indications
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Recurrent gouty attacks
Tophaceous gout Urolithiasis |
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Allopurinal side effects
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Initiation of gout attack (start with colchicine)
Rash Interstitial nephritis Hypersensitivity rxn |
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Management of pseudogout and acute hydroxyapatite arthritis
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Same as gout but no preventative therapy available
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