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Osteoarthritis
Rheumatoid Arthritis
Septic Arthritis
Whitney Dunbar, RN, BSN
Roshini Mathew, RN, BSN
Neeta Monteiro, RN, BSN
Erin Vitale, RN, BSN
November 18, 2013
Objectives
1. Discuss the pathophysiology, etiology, and causative
mechanisms for osteoarthritis, rheumatoid arthritis,
and septic arthritis.
2. Discuss the prevalence of all three conditions.
3. Review signs and symptoms and the differential
diagnoses for these conditions.
4. Examine physical assessment findings and diagnostic
tests specific for these conditions.
5. Determine treatment measures, health promotion, and
disease prevention strategies.
6. Analyze the outcomes associated with the treatments
and other interventions.
7. Consider appropriate follow-up plan for patients with
these conditions.
ARTHRITIS
Osteoarthritis (OA)
Osteoarthritis: Definition
Osteoarthritis is chronic progressive joint failure,
in which all structures of the joint have
undergone pathologic changes
• Hallmark of OA- loss of articular cartilage
• Mild synovial inflammation
• Formation of osteophytes (bony spurs)
• Thickening & sclerosis of subchondral bone
• Stretching of the articular capsule
• Weakness of muscles bridging the joint
• Meniscal degeneration (in knee)
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)
• Localized (1-2 joints)
• Generalized (>3 joints)
Hand Joints Affected by OA
PIP (Bouchard‟s nodes)
DIP (Heberden‟s nodes)
Joints Affected by Osteoarthritis
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
(CDC, 2011)
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 hospitalizations
Mortality: 0.2-0.3 deaths per 100,000 population
due to OA
(CDC, 2011)
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 per patient
• 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
• Wear/tear, metabolic abnormalities,
biomechanical factors
• The bone surfaces become less well protected
by cartilage exposing the nerves
• Pain occurs upon weight bearing and
mobilization between two articulating bones
• Cartilage degradation products are released
into the synovial fluid causing synovial
inflammation
Pathophysiology of Osteoarthritis
• The inflamed synovium contributes to the
formation of osteophytes
• Osteophytes cause malalignment restricting
joint ROM, further damaging cartilage and
underlying bone
• Chronic and acute injuries can start the
disease process
• Consequences of genetic abnormalities, age,
metabolic factors, obesity and some cartilage
is especially vulnerable to OA
Pathophysiology of Osteoarthritis
Pathophysiology of Osteoarthritis
Risk Factors For Osteoarthritis
Risk for OA, Mal-alignment
Clinical Manifestations Of OA
Main symptom of OA
• Pain
• Exacerbated by activity
• Relieved with rest
Clinical manifestations of OA
• Dull aching joint pain exacerbated by activity &
relieved with rest
• Symptoms worsen as the day progresses
• Pain occurs at rest as OA progresses
• Joint stiffness <30 minutes
• Absence of constitutional symptoms
• Increased bony prominence at the joint margins
• Crepitus or a grating sensation upon joint ROM
• Tenderness over the affected joint
• Reduction in joint ROM
Diagnostic Features of OA
• Sign/symptoms: Joint pain that increases with
activity, brief morning stiffness, crepitus, bony
enlargement, & tenderness on palpation
• Pattern of joint involvement
• Absence of constitutional signs and symptoms
• Non-inflammatory synovial fluid (<2000 WBC/mcl)
• ESR normal for age
• Negative serologic test for antinuclear antibody,
anti-CPP, and rheumatoid factor
Diagnostic Features of OA
Radiographic evidence of OA
• Non-uniform joint-space narrowing
• Osteophyte formation
• Lipping of marginal bone
• Thickened, dense subchondral bone (sclerosis)
• Bone cysts
X-ray of Osteoarthritis of Hand
X-ray of Osteoarthritis of the Knee
X-ray of Osteoarthritis of the Hip
Diagnosis of Osteoarthritis
Hand Knee Hip
Hand pain, aching or
stiffness
Knee pain Hip pain
Enlargement of two or
more joints
Radiographic
osteophytes
Two of the following:
• ESR < 10 mm/h
• Radiographic femoral
or acetabular
osteophytes
• Radiographic joint
space narrowing
Fewer than 3 swollen
MCP joints
One of the following:
• Age >50 years
• Morning stiffness <30
minutes
• Crepitus on motion
Two or more DIP joints
enlarged
Deformity in two or more
joints- DIP, PIP, CMC
Examination of Joint Fluid in OA
Differential Diagnosis of OA
• Rheumatoid arthritis
• Psoriatic arthritis
• Gout
• Pseudo gout, Wilson disease
• Osteoporosis
• Metastatic cancer
• Multiple myeloma
Management of Osteoarthritis
• Therapy is not curative
• Symptom management
• Goal of treatment
• Control pain
• Improve function
• Minimize disability
• Enhance health-related quality of life
• To prevent progression of the process
• Patient education
• Minimize the risk of drug-associated toxicity,
particularly with NSAIDs
ACR recommendations for Hand OA
American College of Rheumatology (ACR) 2012
non pharmacological recommendations
• Evaluation by health care provider
• Assess ability to perform ADLs
• Instruct in joint protection techniques
• Provide assistive devices for ADLs
• Use of thermal modalities (Heat/cold)
• Trapeziometacarpal joint splints for OA of the
trapeziometacarpal joint
Trapeziometacarpal joint splints
Joint Protection Techniques Hand OA
Pharmacological Rx for Hand OA
ARC 2012 recommendations
• Topical capsaicin 0.025-0.075% TID or QID
• Topical analgesic
• Depletes substance P & inhibits transmission
of pain impulse
• SE: Pruritus, burning sensation
• ACNP may prescribe
(ACR, 2012)
Pharmacological Rx for Hand OA
• Topical NSAIDs
• Diclofenac gel 1%, 4 g QID (max
16g/joint/day)
• Trolamine salicylate apply QID prn
• Oral NSAIDs, including COX-2 inhibitors
• Naproxen 500 mg PO BID
• Ibuprofen 400-800 PO q6hrs
• Meloxicam 7.5-15 mg PO QD
• Diclofenac 50 mg PO q8hrs
• Celecoxib (COX-2) 100 mg PO BID
• ACNPs may prescribe
(ACR, 2012)
Pharmacological Rx for Hand OA
• >75 years used topical vs oral NSAIDs
• Action: Decreases prostaglandin production,
anti-inflammatory, and analgesic
• SE: GI ulcer, bleeding, HTN, renal failure,
heart failure
• Take with food
• If GI SE Take PPI omeprazole 20-40 mg OD or
• misoprostol 100-200 mcg QID with food
• ACNPs may prescribe
Management of OA: NSAIDs
Pharmacological Rx for Hand OA
• Tramadol 50-100 mg q 6 hours (max 400 mg/day)
• Inhibits ascending pain pathway (analgesic)
• Inhibits norepinephrine & serotonin (anti-depressant)
• SE: Flushing, dizziness, headache, pruritus,
constipation
• ACNP may prescribe yes
In hand OA do not use (No evidence to support)
• Intra-articular therapies
• Opioid analgesics
(ACR, 2012)
Non-pharmacological for Hip/Knee
• Weight loss
• Aerobic and resistance land-based exercise
• Aquatic exercise
• Participate in self-management programs
• Manual therapy + supervised exercise (PT/OT)
• Psychosocial interventions
• Use medially directed patellar taping
• Medial wedged insoles for lateral OA (valgus)
• Lateral wedged subtalar strapped insoles (varus)
• Use thermal agents
• Walking aids (canes/walker)
• Tai chi, acupuncture, TENS (Knee OA)
(ARC, 2012)
Medially directed patellar taping
Medial Wedged Insoles for Lateral
Compartment OA
Lateral Wedge Subtalar Strapped
Insoles for Medial Compartment OA
TENS, Thermal, Acupuncture, Tai Chi
Arthritis Self Management Program
• Known as self-help hands on course
• Workshop, given two hours/week for six weeks
• Techniques to deal with pain, frustration, isolation
• Appropriate exercise for maintaining and improving
strength, flexibility, and endurance
• Appropriate use of medications
• Effective communication with provider & others
• Healthy eating
• Making informed treatment decisions
• Disease related problem solving
• Getting a good nights sleep
• Receive booklet „The Arthritis Helpbook‟
Management of OA Hip/Knee
• 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,
kneeling, squatting)
• Reinforce exercise regimen at each visit
• Use cane on the unaffected side of the injury
• If right knee is affected use cane in left
hand to take pressure off the affected joint
Pharmacologic Rx of Hip/knee OA
• Acetaminophen 325-650 mg q4-6hours PO
(max 4g)
• Action: Inhibits prostaglandins, blocks pain impulse
• SE: Hepatotoxic, anemia
• ACNP may prescribe
• Oral NSAIDs
• Naproxen 500 mg PO BID
• Ibuprofen 400-800 PO q6hrs
• Meloxicam 7.5-15 mg PO QD
• Diclofenac 50 mg q8hrs
• Celecoxib (COX-2) 100 mg PO BID
(ACR, 2012)
Pharmacologic Rx of Hip/knee OA
• Topical NSAIDs (knee only)
• Diclofenac gel 1% , 4 g QID (max is 16 g/joint/day)
• Trolamine salicylate apply 3-4 times/day prn
• Action: Decreases prostaglandin, analgesic, antiinflammatory
• SE: GI ulcer, hypertension, renal failure, thrombocytopenia
• ACNPs may prescribe NSAIDs
• Tramadol 50-100 mg q6h (max 400 mg/day)
• Inhibits ascending pain pathway (analgesic)
• Inhibits norepinephrine & serotonin (anti-depressant)
• SE: Flushing, dizziness, headache, pruritus,
constipation
• ACNP may prescribe tramadol
(ACR, 2012)
Pharmacologic Rx of Hip/knee OA
Intra-articular corticosteroid injections
• Methylprednisolone 40 mg q 12 weeks
• Betamethasone 5.7 mg q 12 weeks
• Triamcinolone 20-40 mg q 12 weeks
• Hydrocortisone 50 mg q 12 weeks
• Action: Reduces inflammation and pain
• Only short term improvement up to 2-4 weeks
• Practitioners refine and individually tailor drug, dosing
regimen to patient need & clinical response
• SE: Deterioration of knee joint , peri capsular
calcification, steroid arthropathy
• Physician initiated or physician consult
(Douglas, 2012)
Pharmacologic Rx of knee OA
If inadequate response to initial therapy (Knee)
• Intra-articular hyaluronate injections
• Hyaluronate acts as a joint lubricant
• Euflexxa: 20 mg (2 ml) once weekly for 3 weeks
• Hyalgan: 20 mg (2 ml) once weekly for 5 weeks
• Orthovisc: 30 mg (2 ml) once weekly for 3-4 weeks
• Supratz: 25 mg (2.5 ml) once weekly for 5 weeks
• Synvisc: 16 mg (2ml) once weekly for 3 weeks
• Synvisc-One: 48 mg (6 ml) once
• Physician initiated or Physician consult
• SE: Erythema, arthralgia, fatigue, nausea
(ACR, 2012)
Pharmacologic Rx of knee OA
If inadequate response to initial therapy (Knee)
• Duloxetine 30 mg once daily PO x 1 week
• Then increase to 60 mg once daily PO
• Action: Inhibitor of serotonin & norepinephrine
• SE: HA, nausea, palpitations, dizziness
• ACNP may prescribe
Pharmacologic Rx of knee OA
If inadequate response to initial therapy (Knee)
• Opioids (Pain/rheumatology/orthopedic Consult)
• Codeine 50 mg PO BID
• Hydrocodone 5 mg PO QID
• Meperidine 50 mg PO q4h
• Morphine 10 mg PO q4h
• Oxycodone 5 mg q4h
• Action: Binds to opioid receptors, inhibit pain
pathway
• SE: Circulatory depression, sedation,
dependence
• Physician consult or physician initiated
Management of Osteoarthritis
Strong Recommendation for opioids
• In patients who are not willing for surgery
• In patients who had contraindications for surgery &
failed initial therapy
Surgical management
• Total hip and knee replacement provides excellent
symptomatic and functional improvement when
severe OA restricts walking or causes pain at rest,
particularly at night.
• Arthroscopy: Repair of joint
• Arthroplasty: Replacement of joint with prosthetic
appliance
Treatment For Osteoarthritis (ACR, 2012)
Non pharmacological Education, exercise, injury prevention, weight loss,
assistive devices, self-managed programs
Pharmacological
Topical NSAIDS
Capsaicin (hand)
Oral
Acetaminophen
NSAIDS &
COX-2 inhibitors
Tramadol
Opioids (if no surgery)
Duloxetine
Injectable Intra-articular corticosteroids hip/knee
Intra-articular hyaluronic acid (knee)
Surgery
Total joint arthroplasty of knee/hip having failed medical
treatment
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
• Osteonecrosis of the knee
• Meniscal tear (knee)
• Gout
• Pseudogout
Prognosis and Prevention of OA
• Prognosis: Leading cause of disability
• Limitation in ADLs
• Decreased ROM
• Increased pain
• Decreased muscle strength
• Comorbidities may worsen disability
• Prevention:
• Patient education
• Weight reduction
• Avoid repeated motions of joint
• Correcting leg length discrepancy of > 1cm with
sole modification may prevent knee OA
• Avoiding major injuries (young athletes)
• Previous injury avoid athletic activities
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
• Monitor effectiveness of medications
• Monitor side effects of drugs
• Evaluate ability to perform ADLs
• Evaluate effectiveness of splints & assistive
devices
• X-rays of affected joint to monitor joint damage
• Assess need for consults: pain consult,
rheumatologist, orthopedic surgeons
Rheumatoid
Arthritis (RA)
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
Rheumatoid Arthritis – Patho Animation Video
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!
)
(Longo et al., 2012)
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 DEFORMITIES
RA of Hands & Feet
RA: Physical Examination Findings
Extra-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: Diagnosis
The 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: Differential Diagnosis
OA vs. RA
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 migransLyme Disease
h
RA: Treatment
• Goals:
• Pain relief
• Reduce inflammation
• Prevent deformity
• Maintain function
• Control systemic involvement
• Therapy is not curative
(ACR, 2012)
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-TNF
MOA: 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)
RA: Pharmacological Treatment
(ACR, 2012)
Biologic DMARDs & Co-morbidities
(ACR, 2012)
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
Glucocorticoid Treatment in RA
(Hoes et al., 2010)
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)
Septic Arthritis (SA)
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
(Hellman & Imboden, 2013).
SA: Modes of Infection
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
• Osteomyelitis
• Metastasis
• Systemic
vasculitis
• Lyme disease
(Cleveland Clinic, 2011).
SA: Differential Diagnosis
Osteomyelitis 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
(Horowitz et al., 2011).
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
Arthrocentesis Procedure Video
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 and daptomycin 6 mg/kg/dose IV once
daily. Some antibiotic options with parenteral and oral
routes of administration include the following: TMP-
SMX 4 mg/kg/dose twice daily in combination with
rifampin 600 mg once daily, linezolid 600 mg twice
daily, and clindamycin 600 mg every 8 h
• Some experts recommend the addition of rifampin 600
mg daily or 300–450 mg PO twice daily to the antibiotic
chosen above. 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
Questions
Question 1
A 52 year old female with a two year history of
weakness is diagnosed with rheumatoid
arthritis. Which of the following statements is not
true regarding rheumatoid arthritis?
A: Rheumatoid arthritis is a chronic inflammatory disease of
the synovial joint and tendon sheath
B: Disease-modifying anti-rheumatic drugs (DMARDs) is
usually first line therapy for rheumatoid arthritis
C: Morning stiffness for more than an hour and joint pain that
improves as the day progresses are characteristic symptoms
of rheumatoid arthritis
D: The cause of rheumatoid arthritis is from repetitive use of
a joint
Question 1
A: Rheumatoid arthritis is a chronic inflammatory
disease of the synovial joint and tendon sheath
B: DMARDs are usually first line therapy for
rheumatoid arthritis
C: Morning stiffness for more than an hour and joint
pain that improves as the day progresses are
characteristic symptoms of rheumatoid arthritis
D: The cause of rheumatoid arthritis is from
repetitive use of a joint
(Longo et al., 2012)
Rationale
A: RA is a chronic inflammatory disease of the
synovial joint and tendon sheath, proximal
interphalangeal and metacarpophalangeal joints
are often affected
B: DMARDs are usually first line of tx for RA and
for severe cases, add anti-TNF with methotraxate
C: Morning stiffness, which lasts several hours,
and joint pain or stiffness are common symptoms
D: Cause is unknown. Joint degeneration and wear
and tear is correlated with OA
(Longo et al., 2012)
Question 2
An ACNP is assessing a 52 year-old female who
complains of pain in her hands in the morning. She
states she frequently drops her car keys and drops
her hairbrush, and feels she sometimes cannot
maintain her grip on items. Xrays of her hands
reveal bilateral, symmetrical soft tissue swelling of
both metacarpals. What laboratory finding will
likely be reported positive to the ACNP?
A: Procalcitonin
B: Antinuclear antibody
C: Anti-cyclic Citrullinated Peptide test
D: Blood cultures
Question 2
A: Procalcitonin
B: Antinuclear antibody
C: Anti-cyclic Citrullinated Peptide test
D: Blood cultures
Rationale:
A: Procalcitonin rises due to proinflammatory stimulus but
not specific to RA
B: ANA not often positive in RA
C: Anti-CCP has a higher sensitivity than RF and is more
likely to be positive early in disease
D: Blood cultures not specific for RA
(Longo et al., 2012; Singh et al., 2012)
Question 3
A 62-year old male presents to the ED complaining of chills and
right knee pain that started yesterday and has progressed in
severity. He states the only physical activity he has done in
the last few days is some work in his garden. Denies falling or
suffering an animal bite. Past medical and surgical history
includes hypertension, hypothyroid, and right total arthroplasty
five months ago. Physical findings include erythema of the
right knee with heat on palpation and limited range of
motion. Vitals: temperature 101.6, HR: 105 bpm, 20 breaths
per minute, and blood pressure 108/78 mmHg. What is this
patient‟s most likely diagnosis?
A: Osteoarthritis
B: Septic Arthritis
C: Rheumatoid Arthritis
D: Gout
Question 3
A: Osteoarthritis
B: Septic Arthritis
C: Rheumatoid Arthritis
D: Gout
Rationale: Patients with SA typically present with
acute onset pain, swelling, heat, and limited
movement of the affected joint. Patients with SA
can present with fever and chills. A risk factor for
SA includes a prosthetic joint.
(Horowitz et al., 2011)
Question 4
Which of the following clinical manifestations is
not associated with osteoarthritis?
A: Heberden's nodes
B: Symptoms are worse in the morning and
improve as the day progresses
C: Morning stiffness is less than 30 minutes
D: Pain is exacerbated by activity and relieved
with rest
Question 4
A: Heberden's nodes
B: Symptoms are worse in the morning and improve
as the day progresses
C: Morning stiffness is less than 30 minutes
D: Pain is exacerbated by activity and relieved with
rest
Rationale: Associated with RA. Symptoms worsen
as the day progresses in OA.
(Papadakis & McPhee, 2013)
Question 5
A 72 year old female patient presents to the office with
complaints of worsening pain and limited range of
motion in her right knee. She was diagnosed with
osteoarthritis of the right knee five years ago. On
radiographic examination of the right knee the ACNP
may expect to see all of the following EXCEPT
A: Thinning subchondral bone
B: Narrowing of the joint space
C: Osteophyte formation and lipping of marginal bone
D: Bone cysts
Question 5
A: Thinning subchondral bone
B: Narrowing of the joint space
C: Osteophyte formation and lipping of marginal
bone
D: Bone cysts
Rationale:
Thickened, dense subchondral bone (not thinning)
is usually noted in OA on radiographic examination.
The other findings are accurately noted on
radiographic examination of the knee.
(Papadakis & McPhee, 2013)
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