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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