Post on 24-Dec-2015
OsteoarthritisRheumatoid Arthritis
Septic Arthritis
Whitney Dunbar, RN, BSNRoshini Mathew, RN, BSNNeeta Monteiro, RN, BSN
Erin Vitale, RN, BSN
Osteoarthritis: Definition
Osteoarthritis is a joint disease mostly affecting middle-age to elderly people and is characterized by
• Minimal articular inflammation• Progressive damage to the articular cartilage • Thickening of subchondral bone & joint capsule• Formation of osteophytes (bony spurs)• Mild synovitis
Classification of Osteoarthritis
Idiopathic (primary) OA• No predisposing cause• Occurs spontaneously• Usually associated with aging
Secondary OA • Occurs due to predisposing factors such as:
trauma, repetitive stress (occupation, sports), congenital abnormality, metabolic disorder, endocrine (DM, obesity), or other bone/joint disease (RA, Gout)
Classification of Osteoarthritis
Subdivided into: • OA of the hip, hand, knee, spine, or foot• Localized (1-2 joints affected)• Generalized (>3 joints affected)• Erosive: Erosion of the distal interphalangeal
joint (DIP) and proximal interphalangeal joints (PIP) of the hand
Osteoarthritis: Prevalence
• Most common form of arthritis• Prevalence increases with age (13.9% >25 years) • 70% of people over the age of 70 have
radiographic features of OA in weight bearing joints• More common in elderly women than men• Leading cause of disability in the elderly
www.cdc.gov
Osteoarthritis: Prevalence
• According to ACR, CDC, NIH (2012)• 27 million Americans are living with OA• Life time risk of developing OA of the knee is
46%• Life time risk of developing OA of the hip is
25%• Secondary OA may occur at any age especially
after joint trauma, chronic inflammatory arthritis, or congenital malformation
Osteoarthritis: Incidence
• Hip OA = 88 per 100,000 person years• Hand OA = 100 per 100,000 person years• Knee = 240 per 100,000 person years • Highest incidence is knee OA
Hospitalizations: OA accounts for 55% of all arthritis-related hospitalizationsMortality: 0.2-0.3 deaths per 100,000 population due to OA
www.cdc.gov
Osteoarthritis: Cost
Cost • $7.9 billion estimated costs of knee and hip
replacements • Average direct costs of OA ~$2,600 per year out-
of-pocket expenses• Total annual disease costs = $5700 (US dollars)
• Job-related OA costs $3.4 to $13.2 billion per year
Pathophysiology of Osteoarthritis
• Articular cartilage: A thin layer of cartilage that covers the bone in a synovial joint
• Function of articular cartilage:• Reduces friction at the
joint• Absorbs shocks
associated with joint use• Transmits weight loads to
the underlying bone
Pathophysiology of Osteoarthritis
• Deterioration of the hyaline articular cartilage due to damage to chondrocytes
• The bone surfaces become less well protected by cartilage exposing the nerve endings on the bone
• Pain occurs upon weight bearing and mobilization between two articulating bones
• Cartilage degradation products are released into the synovial fluid causing synovial inflammation
• The inflamed synovium contributes to the formation of osteophytes at the edge of a joint
Pathophysiology of Osteoarthritis
• Osteophytes cause malalignment restricting joint ROM, further damaging cartilage and underlying bone
• Chronic and acute injuries can start the disease process
• Cartilage matrix turn over, spurred by daily loading across the joint can replenish cartilage
• Consequences of genetic abnormalities, age, metabolic factors not fully understood, and some cartilage is especially vulnerable to OA
Clinical manifestations of OA
• Dull aching joint pain exacerbated by activity and relieved with rest
• Pain occurs at rest as disease progresses• Joint stiffness <30 minutes upon awakening in
the morning or after extended periods of inactivity
• Absence of constitutional symptoms• Increased bony prominence at the joint
margins
Clinical manifestations of OA
• Crepitus or a grating sensation upon joint ROM• Tenderness over the affected joint• Articular gelling- stiffness lasting short periods
and dissipates after initial ROM• Reduction in joint ROM• Symptoms worsen as the day goes on
Diagnostic Features of OA
• Sign/symptoms: Joint pain that increases with activity, brief morning stiffness, crepitus, bony enlargement, & tenderness on palpation over the joint
• Pattern of joint involvement• Absence of constitutional signs and symptoms• Non-inflammatory synovial fluid (<1000
WBC/mcl)• ESR normal for age• Negative serologic test for antinuclear antibody
and rheumatoid factor
Diagnostic Features of OA
• Radiographic evidence of OA• Non-uniform joint-space narrowing• Osteophyte formation• Subchondral cysts• Eburnation (bony sclerosis)
Examination of Joint Fluid in OA Measure Normal Osteoarthritis
Volume <3.5 Often > 3.5
Clarity Transparent Transparent
Color Clear Yellow
WBC <200 200-300
PMN leukocytes <25% <25%
Culture Negative Negative
Glucose Nearly = to serum Nearly = to serum
Differential Diagnosis of OA
• Rheumatoid arthritis• Psoriatic arthritis• Gout• Pseudo gout, Wilson disease• Osteoporosis• Metastatic cancer • Multiple myeloma
Management of Osteoarthritis• Goal of treatment
• Control pain• Improve function• Minimize disability• Enhance health-related quality of life• Minimize the risk of drug-associated toxicity,
particularly with NSAIDs• The American College of Rheumatology (ACR),
2012 has developed recommendations for OA of the hip, knee and hands; other areas have not been developed
Management of Osteoarthritis
• Patient education• Proper positioning and support of back and neck• Adjust furniture, raise chair or toilet seat• Avoid repeated motions of joint (e.g. bending)• Use arthritis support devices for ADLs (walker,
cane)• Use cane on the unaffected side of the injury• Use of thermal modalities • Trapeziometacarpal joint splints for hand OA
Management of Osteoarthritis
• Non pharmacological recommendations ACR, 2012• Evaluate ability to perform ADLs• Weight loss for overweight patients• Participate in aquatic exercise• Start aerobic exercise program• Strengthening exercise to build supporting
muscle• Exercise daily to reduce pain and improve
function• Participate in self-management programs
Management of Osteoarthritis
• Refer to a physical therapist & occupational therapist
• Reinforce exercise regimen at each visit• Consider for knee OA:
• Medially directed patellar taping• Wedged insoles for either medial (valgus
knee) or lateral (varus) compartment OA
Management of OsteoarthritisPharmacological Management, ACR 2012• Topical capsaicin cream 0.025-0.075% TID or QID for
hand OA• Mild disease should start with acetaminophen 325-650
mg q 4-6 hours (max 4g/day) for knee and hip OA• For patients not responding to acetaminophen consider
NSAIDs• Topical NSAIDs
• Diclofenac gel 1% , 4 g QID (max is 16 g/joint/day)• Trolamine salicylate apply 3-4 times/day prn
Management of Osteoarthritis
• Oral NSAIDs• Diclofenac 150-200 mg/day in 3-4 divided doses• Celebrex 200 mg/day OD or divided dose BID
• >75 years use topical vs oral NSAIDs due to GI toxicity• Tramadol 50-100 mg q 6 hours (max 400 mg/day)• Intra-articular corticosteroid injections for hip & knee• Chondroitin sulfate and glucosamine, alone or in
combination did not prove to be effective, therefore not recommended by ACR
Management of Osteoarthritis
• Consultation• Rheumatologist consult for severe symptoms• If diagnosis is doubtful consult • Assistance with needle aspiration or injection• Requiring narcotic analgesics• Severe OA unrelieved by conservative
therapies may require orthopedic consultation and surgery
Management of Osteoarthritis
• Surgical management• Used for severe disability or uncontrolled pain• Arthroplasty: partial or total replacement of
joint with prosthetic appliance• Asthrodesis or laminectomy: fusion of bones,
particularly in spine• Osteoplasty- scraping and lavage of
deteriorated bone
Management of Osteoarthritis
• Surgical management• Osteotomy-changing alignment of bone to
relieve stress on joint• Total hip and knee replacement provides
excellent symptomatic and functional improvement when involvement of that severely restricts walking or causes pain at rest, particularly at night.
Acute Complications of OA
• The development of new symptoms such as abrupt onset of heat, redness, and swelling near the joint, joint locking or giving away may be attributable to active inflammation of adjacent non-articular tissues, including • Regional tendonitis• Bursitis• Ruptured baker cyst• Meniscal tear• Gout• Pseudogout
Prognosis and Prevention of OA
• Prognosis: Symptoms may be quite severe and limit activity considerably especially with involvement of the hips, knees, and cervical spine
• Prevention: • Weight reduction reduces the risk of knee OA• Correcting leg length discrepancy of > 1cm with
sole modification may prevent knee osteoarthritis • Maintaining normal vitamin D levels may reduce
the occurrence and progression of OA
Follow up of Osteoarthritis
• Inform patient to return if symptoms worsen, or if there is no relief of symptoms
• Regular follow-up visit, at least once a year• Ensure symptoms are managed • X-rays of affected joint to monitor joint damage
What is RA?• RA is a chronic, autoimmune, systemic
inflammatory disease• Destruction of synovial membrane leads
to:• Joint pain and swelling • Joint deformity
• Occurs at any age
RA: Disease Course• Monocyclic: Have one episode which
ends within 2-5 years of initial diagnosis and does not reoccur.
• Polycyclic: The levels of disease activity fluctuate over the course of the condition
• Progressive: RA continues to increase in severity and is unremitting
RA: Incidence & Prevalence• 1.5 million adults (≥18) have RA in the US (0.5-
1% of total population)• Women 9.8 per 1000 • Men 4.1 per 1000• 1995-2007: 41 per 100,000 diagnosed each year• Incidence increased with age: 8.7 per 100,000
aged 18-34 vs. 54 per 100,000 aged ≥ 85 years• Highest incidence in 65-74 year olds: 89 per
100,000
(CDC, 2012; Myasoedova et al., 2010)
RA: Etiology
• Cause remains unknown• Inflammatory response may be
related to an infectious agent• Mycoplasma, Epstein-Barr virus
(EBV), cytomegalovirus (CMV), parvovirus, rubella
• May have a genetic predisposition
RA: Pathophysiology
http://www.youtube.com/watch?v=imR4hCwrGmQ
RA: Pathophysiology
• Hyperplasia/hypertrophy of synovial cells• Infiltration of mononuclear cells and CD4+ T cells
(Longo et al., 2012)
RA: Pathophysiology
• Within the synovium, activated lymphocytes, macrophages, and fibroblasts release pro-inflammatory cytokines IFN-y, IL-1, TNF
• Cytokines promote B-cell proliferation which produces auto-antibodies/rheumatoid factor
• Immune-complexes formed and complement activation leads to further inflammation
• PMNs migration, mast cells, and prostaglandins facilitate exudation of inflammatory cells
End Result – INFLAMMATION!
RA: Systemic Damage• Inflamed synovium and cytokines
release degradative enzymes Cartilage/tissue damage
• Activation of osteoclasts Demineralization of bone
• Synovium affected first, then spreads to cartilage, tendons, ligaments
• Soft tissue damage to kidneys, heart, lungs
RA: Subjective Findings• ~66% have gradual onset of
symptoms• Symmetric joint and muscle pain
that is worse in the morning and improves as day progresses
• Pain worse with movement• Swelling and tenderness in
affected joints• Usually hands, wrists, knees,
feet• Weakness, fatigue• Generalized weakness • Anorexia• Weight loss
RA: Physical Examination Findings
Articular
• “Z” deformity – Radial deviation of wrist, ulnar deviation of digits
• Swan-neck deformity – Hyperextension of PIP, flexion of DIP
• Boutonniere deformity – Flexion of PIP, extension of DIP
RA: Physical Examination FindingsExtra-Articular/Systemic
• 40% of patients • Rheumatoid nodules: pleura, meninges • Rheumatoid vasculitis: neuropathy, cutaneous
ulcers (brown spots on nail beds or legs),• Pulmonary: pleuritis , pulmonary nodules
(Caplan’s syndrome), interstitial fibrosis, pulmonary HTN
• Cardiovascular: pericarditis, tamponade, CHF• Eye: Scleritis, Sjögren’s Syndrome (dry eyes)• Felty’s syndrome: splenomegaly,
neutropenia, anemia, thrombocytopenia
RA: Laboratory Findings
• + Rheumatoid Factor• RF present in 70-90% of pts with RA
• + Anti-CCP (anti-cyclic citrullinated peptide) test
• Normochromic, normocytic anemia • Neutropenia• Thrombocytopenia • Eosinophilia • ESR elevated• CRP elevated
RA: DiagnosisThe 2010 American College of Rheumatology/European League
Against Rheumatism classification criteria for rheumatoid arthritis
(ACR/ELAR, 2010)
RA: Radiographic Evaluation
• Xrays• Symmetrical involvement• Articular demineralization • Joint space narrowing• Bone Erosion
• MRIs
(Vasanth, Pavlov, & Bykerk, 2013)
RA: Other Differential Diagnosis• Gouty arthritis: presence of uric acid
crystals in fluid• Viral polyarthritis: rubella, parvovirus,
HBV, HCV• SLE: butterfly rash; ESR elevated but
CRP normal• Polymyalgia Rhematica (PMR): Stiffness
in shoulder, neck, hips; negative RF & anti-CPP
• Fibromyalgia: Pain (not stiffness) in non-articular sites without s/s of inflammation; Negative RF, anti-CCP, ESR, CRP
• Lyme arthritis: tick bite with erythema migrans Lyme Disease
h
RA: Treatment
• Goals:• Pain relief• Reduce inflammation • Prevent deformity• Maintain function• Control systemic involvement
• Therapy is not curative
Synthetic Disease-Modifying Anti-Rheumatic Drugs (DMARDs)
MOA: Decrease acute-phase reactants; Anti-proliferative
ACNPs may prescribe: With MD consult or initiation
• Hydroxychloroquine (Plaquenil®) 200-400mg PO Q D• SE: visual changes, GI distress
• Methotrexate (Rheumatrex®) 7.5mg PO Q wk (titrate by 5mg to max 20 mg/wk)• SE: hepatic/renal failure, bone marrow suppression,
pneumonitis
Immunosuppressants:• Leflunomide (Arava®) 20mg PO Q D
• hepatic failure• Sulfasalazine (Azulfidine®) 2g PO Q D
• hepatic/renal failure
Biologic DMARDs: Anti-TNFMOA: Block cytokine TNF
Side effects: Fatigue, HA, HTN, CHF, hyperlipidemia, reactivation of TB or Hep B, pancytopenia, agranulocytosis, hepatic/renal failure, GI distress, Crohn’s, demyelinating polyneuropathy (GBS), malignancies (lymphoma)
ACNPs may prescribe: With MD consult or initiation
• Adalimumab (Humira®) 40mg SQ Q wk or QOwk• Certolizumab (Cimzia®) 200mg SQ QOwk• Etanercept (Embrel®) 50mg SQ Q wk• Infliximab (Remicade®) 3mg/kg IV Q 8 wks• Golimumab (Simponi®) 50mg SQ Q month
Biologic DMARDs: Non-TNF
Side effects: HA, HTN, malignancies (ALL), reactivation of TB or Hep B, angioedema, bronchospasm, pancytopenia, hyperglycemia, hepatic/renal failure, SJS, arthralgia
ACNPs may prescribe: With MD consult or initiation
• Abatacept (Orencia®) 750mg IV Q month• MOA – Inhibits T-cell activation
• Rituximab (Rituxan®) 1000mg IV Q 6 months• MOA – Depletes B-cells
• Tocilizumab (Actemra®) 4-8mg/kg IV Q month• MOA – Inhibits cytokines (ILs)
NSAIDs in RA• MOA: Decreases prostaglandin production• Side effects: GI ulcer, increased PT, renal failure,
thrombocytopenia• ACNPs may prescribe: Yes
• Symptom relief; Does not alter disease progression• Co-administered with DMARDs therapy• Response may take up to 2 wks
• Naproxen 500mg PO BID• Ibuprofen 400-800mg PO Q 6 hrs• Meloxicam 7.5-15mg PO Q D• Celecoxib (COX-2) 100-200mg PO BID
RA: Non- Pharmacological Treatment
• Interdisciplinary approach• Physical therapy/Occupational therapy• Rest/splinting• Orthotic & assistive devices
Health Promotion/Prevention• Education on disease• Community support (Arthritis Foundation)• Coping with depression/stress• Optimize immune function
RA: Patient Outcomes• Variable• Disease not curable• 19th most common cause for years lost to disability
(CDC, 2010)• Increased likelihood of disability if one of the
following is true:• >20 inflamed joints• High ESR• High titers of RF and anti-CCP• Bone erosions on Xray• Presence of rheumatoid nodules• Advanced age at onset• Presence of comorbid conditions
RA: Patient Outcomes
• Early RA: disability d/t pain & inflammation• Late RA: disability d/t damage to articular
structures• Life expectancy:
• Shortened by 3-7 yrs• 2.5 fold increase in mortality rate• Mortality: 22-30%
• Causes of Mortality in RA:• #1: CVD • #2: Infection• #3: GI Bleeding
(CDC, 2012)
RA: Costs
• $3000 per year in medical costs with RA vs. $1000 with OA
• 2009: 15,600 hospitalizations with RA listed as principal diagnosis • Total hospital charges of $545 million (average
of $35,000 per person)
(AHQR, 2011)
RA: Follow-Up Care
• Evaluate for systemic complications• CXR for respiratory S/S• 2D-Echo for CVD S/S
• Put on ASA 81mg • Ophthalmology consult • Monitor CBC with differential• Dexa-Scan • Xrays of affected joints• Specific lab tests to monitor drug therapy
Self-management Advice to Reduce patients’ CVD Risk in RA
Smoking• Avoid or try to quit smoking
Diet• Try to keep a healthy weight; obesity makes heart disease more likely• Eat a diet rich in fruit, vegetables, low-fat protein (such as poultry, fish, legumes, nuts and seeds, and low-fat dairy), and whole grains• Avoid foods high in sodium, saturated fats, trans fats, and cholesterol
Exercise• Regular exercise and plenty of physical activity are highly recommended
Monitoring of traditional risk factors• Get regular tests for high blood pressure, blood sugar levels, and high cholesterol• Talk to your doctor about your health history, especially if you have a positive family history of heart disease• Get regular checkups
(Palmer & El Miedany, 2013)
What is Septic Arthritis?
• Infection of a joint, typically bacterial
Risk factors are • bacteremia • damaged or prosthetic joints • immunocompromised • Poor skin integrity
• Can involve any joint, but the knee is the most commonly involved accounting for about 50% of the cases
• Usually monoarticular
SA: Incidence & Prevalence
• Incidence of septic arthritis has been estimated at 2 to 10 cases per 100,000 in the general population
• Prevalence of bacterial arthritis among adults presenting with one or a few acutely painful joints approximately 8 to 27 percent
• 30 to 70 cases per 100,000 in patients with rheumatoid arthritis
• The most common mode of spread is hematogenous, with predisposing risk factors
SA: Pathophysiology• Bacteria enters the joint space primarily through
hematogenous spread, as well as direct inoculation and spread from a contiguous infection in soft tissue or bone
• The bacteria initially deposits in the synovial membrane and produces an inflammatory reaction, that is highly neutrophilic, which readily migrates into the synovial fluid
• Synovial membrane hyperplasia develops in 5 to 7 days, and the release of cytokines leads to hydrolysis of proteoglycans and collagen, cartilage destruction, and eventually bone loss
• Direct pressure necrosis due to large synovial effusion results in further cartilage damage
• Happens quickly, significant join damage happens in 1-2 days
SA: Essentials of Diagnosis
• Acute onset of inflammatory monoarticular arthritis, most often in large weight-bearing joints and wrists
• Common risk factors • Infection with causative organisms commonly
found elsewhere in body• Joint effusions are usually large, with white blood
counts commonly > 50,000/mcL
SA: Presentation
• Acute onset• Pain• Swelling• Heat• Limited movement
(PROM & AROM)• Unusual sites, such as
the sternoclavicular or sacroiliac joint, can be involved in injection drug users
• Chills and fever are common
• More than one joint is involved in 15% of cases
• Risk factors for multiple joint involvement include rheumatoid arthritis, associated endocarditis, and infection with group B streptococci
SA sites: knee>hip> shoulder = ankle = wrist
Sternoclavicular septic arthritis accounts for 17% of septic arthritis in intravenous drug users, but only 1% of septic arthritis in the general population
SA: Differential Diagnosis
• Rheumatoid arthritis
• Crystal-induced joint diseases (gout, pseudogout)
• Reactive arthritis• Osteoarthritis• Trauma• Viral arthritis• Lyme disease
• Osteomyelitis• Endocarditis• Metastasis• Systemic vasculitis
SA: Differential DiagnosisOsteomyelitis SA
Subacute onset of limp / non-weight bearing / refusal to use limb
Acute onset of limp / non-weight bearing / refusal to use limb
Localized pain and pain on movement
Pain on movement and at rest
Tenderness Limited range / loss of movement
Soft tissue redness / swelling may not be present & may appear late
Soft tissue redness / swelling often present
+/- Fever Fever
(Grad & Matloff, 2012).
SA: Assessment & Diagnosis
• Thorough H&P• Intraarticular versus periarticular location• Laboratory evaluation
• CBC with differential• ESR• CRP• Blood cultures (positive in 50% patients)• Testing for N. gonorrheae
• Synovial fluid analysis• Imaging
SA: Assessment & Diagnosis
Synovial fluid analysis• Gram Stain• Culture• Leukocyte Count with
Differential• Crystal examination Results:• Elevated WBC count –
usually >50,000• Gram stain generally
positive in 1/3 of cases• Cultures positive in 25-80%
• Radiographic Imaging• XR• CT• MRI
Not always essential, but can help evaluate for complicating factors
FYI: Septic arthritis can coexist with crystal arthropathy; therefore, the presence of crystals does not preclude a diagnosis of septic arthritis (Horowitz et al., 2011).
SA: Arthrocentesis
http://www.youtube.com/watch?v=8adxsdiaAeE
Organisms of Septic Arthritis
Isolates, Number (% total)
Gram positive Staphylococcus aureus 1066 (44) Staphylococci, coagulase negative 84 (3) Streptococci Streptococcus pyogenes 183 (8) Streptococcus pneumoniae 156 (6) Streptococcus agalactiae 69 (3) Other streptococci 104 (4)
Gram negative Escherichia coli 91 (4) Haemophilus influenzae 104 (4) Neisseria gonorrhoeae 77 (3) Neisseria meningitidis 28 (1) Pseudomonas aeruginosa 36 (1) Salmonella spp 25 (1) Other gram-negative rods 110 (5) Miscellaneous (including anaerobes) 136 (6) Polymicrobial 33 (1) (Grad & Matloff, 2012)
.
Clinical Presentations of Septic Arthritis
Clinical History Joint Involvement Pathogen
Cleaning fish tank Small joints Mycobacterium marinum
Dog/cat bite Small joints Capnocytophaga species, Pasteurella multocida
Unpasteurized dairy products Sacroiliac joint Brucella species
IV Drug use Axial joints P. aeruginosa, S. aureus
Stepped on nail Foot P. Aeruginosa
Sexual activity Tenosynovial components Neisseria gonorrhoeae
Soil exposure Knee, hand, wrist Nocardia species, Pantoea agglomerans, sporothrix schenckii
SW US, central & SA knee Coccidoides immitis
SLE ---- N. gonorrhoeae, Proteus species, Salmonella species
Terminal complement deficiency Tenosynovial component in hands, wrists, or ankles
N. gonorrhoeae
(Horowitz et al., 2011).
SA: Treatment
• Combination: Antibiotic therapy + drainage of infected joint
• Rapid initiation of broad-spectrum antibiotics and narrow with culture results if possible• Third-generation cephalosporin: ceftriaxone, 1 g
intravenously daily (or every 12 hours if concomitant meningitis or endocarditis is suspected) OR cefotaxime, 1 g intravenously every 8 hours; OR ceftazidime, 1 g intravenously every 8 hours
• Vancomycin (1 g intravenously every 12 hours, adjust for age, weight, and renal function) should be used whenever MRSA is likely
• The duration of antibiotic therapy is usually 4-6 weeks
SA: Treatment
• IDSA Guidelines for Septic Arthritis by MRSA• Drainage should always be performed• 3-4 week course• Antibiotics available for parenteral administration include• IV vancomycin (B-II) and daptomycin 6 mg/kg/dose IV once
daily (B-II). Some antibiotic options with parenteral and oral routes of administration include the following: TMP-SMX 4 mg/kg/dose (TMP component) twice daily in combination with rifampin 600 mg once daily (B-II), linezolid 600 mg twice daily (B-II), and clindamycin 600 mg every 8 h (B-III)
• Some experts recommend the addition of rifampin 600 mg daily or 300–450 mg PO twice daily to the antibiotic chosen above (B-III). For patients with concurrent bacteremia, rifampin should be added after clearance of bacteremia
SA: Treatment
• Treatment duration and route of administration should be adjusted based on • Any local or systemic factors contributing to
impairment of immune activity• The antibiotic susceptibility of the organism• Concomitant bacteremia or other infection • The overall clinical picture
SA: Treatment
• Early consults• Effective drainage is
usually achieved through early arthroscopic lavage and debridement together with drain placement
• Surgical drainage should be performed when• Conservative treatment fails• Osteomyelitis requires
debridement
• Pain management
• Immobilization with a splint and elevation initially
• Active motion exercises within the limits of tolerance will hasten recovery (PT/OT)
SA: Prevention
• No evidence that patients with prosthetic joints undergoing procedures should receive antibiotic prophylaxis to prevent joint infection unless the patient has a prosthetic heart valve or the procedure requires antibiotics to prevent a surgical site infection
• Education, education, education
• The American Academy of Orthopedic Surgeons advocates prescribing antibiotic prophylaxis for any patient with a prosthetic joint replacement undergoing a procedure that can cause bacteremia or with risk factors
• Case by case basis in conjunction with orthopedic surgeon
SA: Prognosis
• The outcome depends on• Prior health of the patient• The causative organism • The promptness of treatment
• SA can result in joint destruction and immobility• Failure to initiate appropriate antibiotic therapy
within the first 24 to 48 hours of onset can cause subchondral bone loss and permanent joint dysfunction and damage
SA: Discharge
• Patients with SA may be DC’d once there is significant improvement in symptoms and follow-up has been arranged with orthopedic surgery, ID, & PCP
• Depending on the clinical scenario, the patient may require continued parenteral antibiotics
• Education driven by etiology of SA; drug counseling etc.
• Need aggressive PT • May require discharge to
rehabilitation or to home with HHC
References • Agency for Healthcare Quality and Research (AHQR). (2011). HCUPnet: National and regional
estimates on hospital use for all patients from the HCUP Nationwide Inpatient Sample (NIS). National statistics - principal procedure only. ICD-9-CM 714.0-714.9. Retrieved from: http://hcupnet.ahrq.gov/HCUPnet.jsp
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