Osteoarthritis Rheumatoid Arthritis Septic Arthritis Whitney Dunbar, RN, BSN Roshini Mathew, RN, BSN...

Osteoarthritis Rheumatoid Arthritis Septic Arthritis Whitney Dunbar, RN, BSN Roshini Mathew, RN, BSN Neeta Monteiro, RN, BSN Erin Vitale, RN, BSN

Transcript of Osteoarthritis Rheumatoid Arthritis Septic Arthritis Whitney Dunbar, RN, BSN Roshini Mathew, RN, BSN...

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

Normal Joint vs Osteoarthritis

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

Hand Joints Affected by OA

Severe OA of the Hands DIP (Heberden’s nodes) PIP (Bouchard’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


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


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

Pathophysiology of Osteoarthritis

Risk Factors For Osteoarthritis

Risk For Osteoarthritis, 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 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


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)

X-ray of Osteoarthritis of the Hand

X-ray of Osteoarthritis of the Knee

X-ray of the Knee with medial OA

X-ray of Osteoarthritis of the Hip

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

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• 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

Trapeziometacarpal joint splints

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

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


(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


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


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


• “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 of Hands & Feet

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: 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 migrans Lyme Disease


RA: Treatment

• Goals:• Pain relief• Reduce inflammation • Prevent deformity• Maintain function• Control systemic involvement

• Therapy is not curative

RA: Pharmacological Treatment

(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,


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)

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

(Cleveland Clinic, 2011).

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

(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


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


• 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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References• Hellmann D.B., Imboden J.B. (2013). Chapter 20. Rheumatologic &

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