Download Diagnosis, Management, and Treatment of Osteoarthritis

Osteoarthritis
Rheumatoid Arthritis
Septic Arthritis
Whitney Dunbar, RN, BSN
Roshini Mathew, RN, BSN
Neeta Monteiro, RN, BSN
Erin Vitale, RN, BSN
ARTHRITIS
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
www.cdc.gov
Osteoarthritis: Prevalence
• According to ACR, CDC, NIH (2012)
• 27 million Americans are living with OA
• Life time risk of developing OA of the knee
is 46%
• Life time risk of developing OA of the hip is
25%
• Secondary OA may occur at any age
especially after joint trauma, chronic
inflammatory arthritis, or congenital
malformation
Osteoarthritis: Incidence
•
•
•
•
Hip OA = 88 per 100,000 person years
Hand OA = 100 per 100,000 person years
Knee = 240 per 100,000 person years
Highest incidence is knee OA
Hospitalizations: OA accounts for 55% of all
arthritis-related hospitalizations
Mortality: 0.2-0.3 deaths per 100,000 population
due to OA
www.cdc.gov
Osteoarthritis: Cost
Cost
• $7.9 billion estimated costs of knee and hip
replacements
• Average direct costs of OA ~$2,600 per year
out-of-pocket expenses
• Total annual disease costs = $5700 (US
dollars)
• Job-related OA costs $3.4 to $13.2 billion per
year
Pathophysiology of Osteoarthritis
• Articular cartilage: A thin
layer of cartilage that
covers the bone in a
synovial joint
• Function of articular
cartilage:
• Reduces friction at the
joint
• Absorbs shocks
associated with joint
use
• Transmits weight loads
to the underlying bone
Pathophysiology of Osteoarthritis
• Deterioration of the hyaline articular cartilage
due to damage to chondrocytes
• The bone surfaces become less well
protected by cartilage exposing the nerve
endings on the bone
• Pain occurs upon weight bearing and
mobilization between two articulating bones
• Cartilage degradation products are released
into the synovial fluid causing synovial
inflammation
• The inflamed synovium contributes to the
formation of osteophytes at the edge of a
joint
Pathophysiology of Osteoarthritis
• Osteophytes cause malalignment restricting
joint ROM, further damaging cartilage and
underlying bone
• Chronic and acute injuries can start the
disease process
• Cartilage matrix turn over, spurred by daily
loading across the joint can replenish
cartilage
• Consequences of genetic abnormalities, age,
metabolic factors not fully understood, and
some cartilage is especially vulnerable to OA
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
margins
Clinical manifestations of OA
• Crepitus or a grating sensation upon joint
ROM
• Tenderness over the affected joint
• Articular gelling- stiffness lasting short
periods and dissipates after initial ROM
• Reduction in joint ROM
• Symptoms worsen as the day goes on
Diagnostic Features of OA
• Sign/symptoms: Joint pain that increases
with activity, brief morning stiffness,
crepitus, bony enlargement, & tenderness on
palpation over the joint
• Pattern of joint involvement
• Absence of constitutional signs and
symptoms
• Non-inflammatory synovial fluid (<1000
WBC/mcl)
• ESR normal for age
• Negative serologic test for antinuclear
antibody and rheumatoid factor
Diagnostic Features of OA
• Radiographic evidence of OA
• Non-uniform joint-space narrowing
• Osteophyte formation
• Subchondral cysts
• Eburnation (bony sclerosis)
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
•
•
•
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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 Osteoarthritis
Pharmacological Management, ACR 2012
• Topical capsaicin cream 0.025-0.075% TID or QID
for hand OA
• Mild disease should start with acetaminophen 325650 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
100,000
(CDC, 2012; Myasoedova et al., 2010)
RA: Etiology
• Cause remains unknown
• Inflammatory response may be
related to an infectious agent
• Mycoplasma, Epstein-Barr virus
(EBV), cytomegalovirus (CMV),
parvovirus, rubella
• May have a genetic predisposition
RA: Pathophysiology
http://www.youtube.com/watch?v=imR4hCwrGmQ
RA: Pathophysiology
• Hyperplasia/hypertrophy of synovial cells
• Infiltration of mononuclear cells and
CD4+ T cells
(Longo et al., 2012)
RA: Pathophysiology
• Within the synovium, activated lymphocytes,
macrophages, and fibroblasts release proinflammatory 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 of Hands & Feet
RA: Physical Examination Findings
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•
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 migrans
h
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 AntiRheumatic 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
•
•
•
•
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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
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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
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Interdisciplinary approach
Physical therapy/Occupational therapy
Rest/splinting
Orthotic & assistive devices
Health Promotion/Prevention
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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
SA: Modes of Infection
(Hellman & Imboden, 2013).
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).
Sternoclavicular septic
arthritis accounts for
17% of septic arthritis
in intravenous drug
users, but only 1% of
septic arthritis in the
general population
SA sites: knee>hip>
shoulder = ankle =
wrist
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 Diagnosis
Osteomyelitis
SA
Subacute onset of limp / non- Acute onset of limp / nonweight bearing / refusal to
weight bearing / refusal to
use limb
use limb
Localized pain and pain on
movement
Pain on movement and at
rest
Tenderness
Limited range / loss of
movement
Soft tissue redness / swelling Soft tissue redness / swelling
may not be present & may
often present
appear late
+/- 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 2580%
• 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
http://www.youtube.com/watch?v=8adxsdiaAeE
Organisms of Septic Arthritis
Isolates, Number (% total)
Gram positive
Staphylococcus aureus 1066 (44)
Staphylococci, coagulase negative 84 (3)
Streptococci
Streptococcus pyogenes 183 (8)
Streptococcus pneumoniae 156 (6)
Streptococcus agalactiae 69 (3)
Other streptococci 104 (4)
Gram negative
Escherichia coli 91 (4)
Haemophilus influenzae 104 (4)
Neisseria gonorrhoeae 77 (3)
Neisseria meningitidis 28 (1)
Pseudomonas aeruginosa 36 (1)
Salmonella spp 25 (1)
Other gram-negative rods 110 (5)
Miscellaneous (including anaerobes) 136 (6)
Polymicrobial 33 (1)
(Grad & Matloff, 2012)
Clinical Presentations of Septic Arthritis
Clinical History
Joint Involvement
Pathogen
Cleaning fish tank
Small joints
Mycobacterium marinum
Dog/cat bite
Small joints
Capnocytophaga species,
Pasteurella multocida
Unpasteurized dairy products
Sacroiliac joint
Brucella species
IV Drug use
Axial joints
P. aeruginosa, S. aureus
Stepped on nail
Foot
P. Aeruginosa
Sexual activity
Tenosynovial components
Neisseria gonorrhoeae
Soil exposure
Knee, hand, wrist
Nocardia species, Pantoea
agglomerans, sporothrix
schenckii
SW US, central & SA
knee
Coccidoides immitis
SLE
----
N. gonorrhoeae, Proteus
species, Salmonella species
Terminal complement deficiency
Tenosynovial component in hands,
wrists, or ankles
N. gonorrhoeae
(Horowitz et al., 2011).
SA: Treatment
• Combination: Antibiotic therapy + drainage of
infected joint
• Rapid initiation of broad-spectrum antibiotics
and narrow with culture results if possible
• Third-generation cephalosporin: ceftriaxone, 1 g
intravenously daily (or every 12 hours if
concomitant meningitis or endocarditis is
suspected) OR cefotaxime, 1 g intravenously every
8 hours; OR ceftazidime, 1 g intravenously every 8
hours
• Vancomycin (1 g intravenously every 12 hours,
adjust for age, weight, and renal function) should be
used whenever MRSA is likely
• The duration of antibiotic therapy is usually 4-6
weeks
SA: Treatment
• IDSA Guidelines for Septic Arthritis by MRSA
• Drainage should always be performed
• 3-4 week course
• Antibiotics available for parenteral administration
include
• IV vancomycin (B-II) and daptomycin 6 mg/kg/dose IV
once daily (B-II). Some antibiotic options with
parenteral and oral routes of administration include
the following: TMP-SMX 4 mg/kg/dose (TMP
component) twice daily in combination with rifampin
600 mg once daily (B-II), linezolid 600 mg twice daily
(B-II), and clindamycin 600 mg every 8 h (B-III)
• Some experts recommend the addition of rifampin 600
mg daily or 300–450 mg PO twice daily to the antibiotic
chosen above (B-III). For patients with concurrent
bacteremia, rifampin should be added after clearance
of bacteremia
SA: Treatment
• Treatment duration and route of
administration should be adjusted based on
• Any local or systemic factors contributing
to impairment of immune activity
• The antibiotic susceptibility of the
organism
• Concomitant bacteremia or other infection
• The overall clinical picture
SA: Treatment
• Early consults
• Effective drainage is
usually achieved through
early arthroscopic
lavage and debridement
together with drain
placement
• Surgical drainage should
be performed when
• Conservative treatment
fails
• Osteomyelitis requires
debridement
• Pain management
• Immobilization with a
splint and elevation
initially
• Active motion exercises
within the limits of
tolerance will hasten
recovery (PT/OT)
SA: Prevention
• No evidence that patients • The American Academy
of Orthopedic Surgeons
with prosthetic joints
advocates prescribing
undergoing procedures
antibiotic prophylaxis for
should receive antibiotic
any patient with a
prophylaxis to prevent
prosthetic joint
joint infection unless the
replacement undergoing
patient has a prosthetic
a procedure that can
heart valve or the
cause bacteremia or
procedure requires
with risk factors
antibiotics to prevent a
• Case by case basis in
surgical site infection
conjunction with
• Education, education,
orthopedic surgeon
education
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 followup 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
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