RaeAnne Fondriest, RN, BSN - PowerPoint Presentation

Slide1

RaeAnne Fondriest, RN, BSNKatie Kearney, RN, BSNMichelle Nissen, RN, BSNAngela Robinson, RN, BSNTeresa Siefke, RN, BSN

Diagnosis, Prevention and

Management:

Osteoarthritis

Rheumatoid Arthritis

Septic ArthritisSlide2

ObjectivesIdentify prevalence of arthritic conditionsDiscuss the pathophysiology of arthritic conditionsRecognize physical assessment attributes of arthritic conditions Discuss current treatment guidelines for arthritic conditionsIdentify preventative strategies of arthritic conditions

Outline needed follow up for the treatment of arthritic conditions Slide3

OsteoarthritisSlide4

Pathophysiology

(Ling et al., 2009)Slide5

Causative AgentsOld AgeObesityImproper joint alignmentDirect or repetitive trauma

Genetic abnormalities

(Keenan et al., 2012)Slide6

PrevalenceOsteoarthritis affects 13.9% of the population over the age of 25 and 33.6% over the age 65Job related costs from AO average 3.4 to 13.2 billion per year OA of the knee is one of the top 5 leading causes of disability among adultsHospitalizations: OA accounts for 69.9% of arthritis related hospitalizations

The rate of total knee replacement and total hip replacement increased by 187% and 86.2% from 1991 to 2007

The estimated costs due to hospital expenditures of TKR and THR average 28.5 billion and 13.7 billion in 2009

(Centers for Disease Control and Prevention, 2014) Slide7

Signs and Symptoms Early stages of diseaseEarly morning stiffness of less then 30 minutes

Middle stages of disease

Pain with activity

Improves with rest

Later Stage of Disease

Pain with rest and sleep

Limited Range of motion

(Ling et al., 2009) Slide8

Physical AssessmentSubtle prominence of the finger jointsHerberden’s NodesBouchard’s Nodes

Adapted from: American College Of Rheumatology 2014 Osteoarthritis:

Heberden’s

and Bouchard’s Nodes, Fingers Retrieved from http://http://images.rheumatology.org/viewphoto.php?albumId=77030&imageId=2897683 201411011813361594496608Slide9

Physical AssessmentEffusion of the kneeBony prominenceJoint laxity or unexpected mobility

Mal-alignment of the joint

Varus

or

valgus

deformity

(Ling et al., 2009) Slide10

Differential DiagnosisRheumatoid arthritis Crystalline diseases: Gout, calcium pyrophosphate deposition disease and hyproxyappetiteSeronegative

spondyloarthropathy

:

Psoriatic arthritis and

Rieter’s

Polymyalgia

rheumatica

Bone disease:

Osteomalacia,

hypovitaminosis

D and Paget’s disease

Malignancy:

Myeloma

and metastatic

(Ling et al., 2009)Slide11

Differential DiagnosisInfectious disease: Infectious arthritis, osteomyelitis and sepsis syndromePeriarticular soft-tissue abnormalities: Tendonitis and bursitisNeuromuscular diseases: Neuropathy Systemic disease:

Diabetes, autoimmune-lupus vasculitis

(Ling et al., 2009)Slide12

Diagnostic CriteriaConventional RadiologyOptical Coherence Tomography

(Braun & Gold, 2012;

Sinusas

, 2012)

Hand

Knee

Hip

Hand pain, aching or stiffness

Knee pain

Hip pain

and

and

and

Hand tissue enlargement of

2 or more joints

Radiographic

osteophytes

2 or more of the following:

Fewer than 3 swollen MCP joints

and

ESR <10 mm/

h

and

1 or more of the following:

Radiographic

femoral or

acetabular

osteophytes

2 or more DIP joints

with hand tissue enlargement

Age ≥ 50

Radiographic joint space narrowingorMorning stiffness <30 minDeformity in 2 or more select jointsCreptus on motion

Ultrasound

MRISlide13

Treatment(

Sinusas

, 2012)Slide14

Knee SurgeryTransplantation of autologous chondrocytes: Used to repair discrete defects in articulate cartilageArthroscopy with debridement:

Allows visualization of the joint and is appropriate for patients with mechanical problems such as locking and giveaway weakness while awaiting more definitive treatment.

Osteotomy:

Transfers the load to the unaffected part of the knee- high tibial osteotomy effective for OA for patients with a single compartment of a varus malaligned knee

Arthroplasty:

Including unicompartment, patellafemoral, total joint in which they replace the damaged cartilage with metal or plastic

(Ling et al., 2009) Slide15

Hip SurgeryArthroscopy: Used to debride

labral

tears, loose body removal,

osteophyte

resection, biopsy,

synovectomy

, or lengthening or releasing of

iliopsoas

or IT band

Osteotomy:

Cutting the bone of the femur or pelvis to realign and fix the bone with plates or screws

Resection

arthroplasty

:

Complete resection of the femoral head without replacement, salvage procedure for severe hip infection resistant to antibiotics or failed total hip

arthroplasty

with

unreconstructable

bone defects

(

Srinivasan

,

Tolhurst

,

Vanderhave

, & Doherty, 2010) Slide16

Hip SurgeryArthrodesis:

realigns the hip to 5 to 10 degrees of external rotation and 20 to 30 degrees of flexion and neutral adduction,

Total Hip and

hemiarthroplasty

:

replacement of the femoral head and or

acetabulum

with manufactured components

Resurfacing

arthroplasty

:

replacement of an

acetabular

component in addition to resurfacing the femoral head with resection of the entire femoral head

(

Srinivasan

,

Tolhurst

,

Vanderhave

, & Doherty, 2010) Slide17

Post Op CarePain management with multimodal strategies including Epidural or spinal analgesiaFemoral nerve blockPeriarticular

injections

Patient controlled analgesia

Oral analgesics

(

Maheshwari

, Blum,

Shekhar

,

Ranawat

, &

Ranawat

, 2009) Slide18

Post Op CareDeep Vein ProphylaxisAssess for history of bleeding disorders or liver diseaseDiscontinue all antiplatelet agents prior to surgery

Use of pharmacological and non-pharmacological devices with high risk patients

Mechanical compressive devices with low risk patients and bleeding disorders

Practice early mobilization following surgery

Use epidural,

intrathecal

and spinal anesthesia to limit blood loss

(Jacobs et al., 2011) Slide19

Post Op Care Infection prevention: Antibiotics within one hour of surgical incisionA first or second generation Cephalosporin – cefazolin or cefuroxime

with

isoxazolyl

penicillin for a substitute

Clindamycin

or

Vancomycin

should be used in patients with penicillin allergies

Vancomycin

should be used in patients who are carriers for MRSA

Patients with previous joint infections should be treated with the same antibiotics effective for that infection

Patients should not receive antibiotics for more than 24 hours post surgery

(Hansen et al., 2014) Slide20

Health PromotionWeight LossRegular ExerciseDietProper use of pain medication

Smoking cessation

Immunization status

(Stein, 2011)Slide21

PreventionPrevention of the need for surgery in osteoarthritis Weight loss: Every one pound of weight loss results in a fourfold reduction in the load exerted on the knee per step (Ling et al., 2009) Prevention of joint injury: Improve mechanical efficiency for occupations with repetitive motion, and reduce joint injury in recreational sports with proper technique and education

Estrogen deficiency: Replacement may reduce the risk of OA

C-reactive protein : higher levels increase risk

(Centers for Disease Control and Prevention, 2014)

Slide22

Outcomes

(

Cushner

,

Agnelli

, Fitzgerald, & Warwick, 2010)Slide23

OutcomesStatistics for total knee and hip arthroplasty85-90% of patients report a good outcome with absence of painPeriprosthetic joint infection rate 1.6-2.3%

Pulmonary Embolism rate 0.5 to 0.9%

Wound infection rates 0.3 to 1.0%

Bleeding and hematoma 0.94 to 1.7%

90 day death rate 0.7 to 2.7%

(Agency For Health Care Research And Quality, 2014) Slide24

Follow Up Depends on the patient progression and amount of external support the patient receives in the way of physical therapy, home nurse visits, home caregivers, and the home environmentFirst follow up visit in 10 to 14 days for suture removalTotal hip replacement follow up is at two weeks, six weeks and 12 weeksFollow up yearly for all joint replacement for first five years

(Skinner & McMahon, 2014) Slide25

Rheumatoid ArthritisSlide26

Prevalence of RAAffects approximately 1% of the world populationWomen 1.06%

vs

men 0.61%

Peak incidence in women 55-64 years of age

Peak incidence in men 75-84 years of age

Associated g

enetic link to RA

Highest prevalence:

American Indian

Alaskan Indian tribes

(Carmona et al., 2002; U.S. Department of Health and Human Services, 2012)Slide27

Prevalence Globally of RA(Shah & Clair, 2012)Slide28

(Google Images, 2014)

Prevalence of Rheumatoid ArthritisSlide29

PathophysiologySystemic chronic autoimmune disease causing inflammation of the connective tissue that affects synovial tissue, cartilage and bones.Early disease Synovium becomes markedly

hyperplastic

and edematous.

Progression of RA

Activation and recruitment of T cells into the joint result in a complex cascade of inflammatory responses.

Accumulation of inflammatory cells,

panus

formation, localized osteoporosis, bony erosions, and destruction of

periarticular

structures.

(Young, 2009)Slide30

Pathophysiology Rheumatoid synovitis is accompanied by the accumulation of inflammatory joint fluid with elevated white cell count Proteins that have been implicated in the inflammatory process:

Proinflammatory

cytokines interleukins

Tumor necrosis factor

Metalloproteinases

transforming growth factor-

β

Granulocyte colony-stimulating factor

Activated complement components

(Young, 2009)Slide31

Pathophysiology(Google Images, 2014)Slide32

2010 Joint Classification Criteria

(

Aletaha

et al., 2010)Slide33

2010 Joint Classification CriteriaAt least 1 joint with definite clinical synovitis (swelling) Synovitis not better explained by another disease

A

score of 6/10 is needed for

RA

classification

(

Aletaha

et al., 2010; Google Images, 2014)Slide34

Early Disease PresentationCommon symptoms:Morning stiffness > 60 minutes

ROM improves with activity

Fatigue

Low-grade fevers

Symmetric arthritis

Rheumatoid nodules

Radiographic changes

Mild weight loss

Most frequently involved joints:

Wrist

Metacarpophalangeal

(MCP)

Proximal

interphalangeal

(PIP)

(Shah & St. Clair, 2012; Google Images, 2014) Slide35

Progressive deformity and decrease in ROMJoint swelling and/or tendernessEarly manifestations usually start in the small bones:HandsFeetFlexor tendon

tenosynovitis

Reduced grip strength and ROM

“Trigger Finger”

(Shah & St. Clair, 2012; Google Images, 2014)

Physical AssessmentSlide36

Progression of Physical AssessmentLate manifestations progress to larger bone involvement and increased debilityTemporal mandibular

joint

Atlantoaxial

cerval

spine

Compressive

myelopathy

and neurological dysfunction

Compression of C1 on C2

These complications have decreased significantly due to treatment

(Shah & St. Clair, 2012) Slide37

Extraarticular Manifestations Arise in active, untreated or inadequately treated disease Affects multiple organ systemsCan occur prior to arthritic symptomsOccurs more in smokers

Early onset disability

Will test positive for serum rheumatoid factor

(Shah & St. Clair, 2012) Slide38

(Shah & St. Clair, 2012) Extraarticular Manifestations Slide39

Extraarticular Manifestations Skin: nodules - extensor surfaces, pressure pointsBone: osteoporosisBlood: anemia, Felty’s syndrome, lymphoma, leukemia

Eyes:

scleritis

,

episcleritis

,

keratoconjunctivitis

sicca

– secondary

Sjögren

syndrome

Heart: CAD, atherosclerosis, MI, pericarditis,

myocarditis

, cardiomyopathy, mitral regurgitation

Peripheral neuropathyRheumatoid vasculitis

Neuro

: cervical

myelopathy

Endocrine:

hypoandrogenism

(Shah & St. Clair, 2012) Slide40

Extra-articular Manifestations Lungs:

Interstitial lung disease

Bilateral infiltrates

Honeycomb pattern

PFTs

– Restrictive pattern

Fibrosis

Bronchiectasis/Bronchiolitis

Rheumatoid nodules

Solitary

Multiple

Often in conjunction with

cutaneous

nodules

Exudative

pleural effusions

(Shah & St. Clair, 2012; Google Images, 2014) Slide41

Differential DiagnosisInfectious arthritisParvovirus B19 (Fifth disease)Hepatitis B or CInfective endocarditisMycobacterium tuberculosisSeptic arthritisLyme disease

Reactive arthritis

Multicentric

reticulocytosis

(Shah & St. Clair, 2012) Slide42

Differential DiagnosisOsteoarthritisGout/PseudogoutPsoriatic arthritisAnkylosing spondylitis

Inflammatory bowel disease

Fibromyalgia

Lupus

Hypothyroidism

Polymyalgia

rheumatica

Sarcoidosis

(Shah & St. Clair, 2012) Slide43

Diagnostic Laboratory Studies Anti-cyclic citrullinated peptide antibody (ACPA or anti-CCP) Helps confirm diagnosis and prognosis, high sensitivity, positive earlier than RF

Rheumatoid factor (RF)

Useful in differentiating RA from other chronic inflammatory

arthritides

C-reactive protein and erythrocyte sedimentation rate 

Assess disease activity

Synovial aspirate

Inflammatory changes and white blood cells

(Nicoll,2012)Slide44

Treatment and MonitoringNSAIDS and High Dose SalicylatesPain and mild inflammation, do not alter disease courseMonitor:

Bleeding

Renal toxicity

GI distress

Avoid in pregnancy

(The Medical Letter, 2012)Slide45

Treatment and MonitoringDisease Modifying Antirhematic Drugs (DMAD) Corticosteroids

Methotrexate

(

Trexall

),

leflunomide

(

Arava

)

sulfasalazine

(

Azulfidine

)

Hydroxychloroquine

(

Plaquenil) - Antimalarial Monitor:

GI Distress

Increased risk for infection

Heptotoxicity

Aplastic

anemia

Agranulocytosis

Steven’s Johnson’s Syndrome

(The Medical Letter, 2012)Slide46

Treatment and MonitoringBiologic Response Modifiers (TNF - inhibitors)

Newer class that target pathways responsible for progression and symptoms of RA

Etanercept

(Enbrel),

Inflixmab

(

Remicade

),

Adalimumab

 (

Humira

)

Montior

:

TB

Hep

B

Infection

Avoid in heart failure

Avoid in

demyelinating

disease

Avoid in pregnancy

(The Medical Letter, 2012)Slide47

Health Promotion and PreventionImmune system suppression awarenessMust check for TB prior to drug initiationRoutine assessment for infection, hypertension, hepatic dysfunction and pulmonary abnormalitiesVision screening

Pregnancy screening prior to treatment

Plaquenil

only DMAD approved in pregnancy

Vaccination

Must immunize against influenza, pneumonia, hepatitis B and herpes zoster

Live vaccines should be given one month prior to treatment

(The Medical Letter, 2012)Slide48

Health Promotion and PreventionRoutine assessment:Cardiac40% of RA patients die from cardiovascular diseaseIncreased risk for MI and stroke due endothelial dysfunctionPulmonary

Skin

Osteoporosis

Smoking cessation

Weight management

(

Dhawan

&

Quyyumi

, 2008)Slide49

Outcomes and Follow UpRoutine monitor of LFTs, CBC and CreatinineMonitor once a month for first 6 months, then every 6 to 8 weeks Monitor general health concerns, comorbidities and quality of life Assess medication doses and monitor for side effects

(

Dhawan

&

Quyyumi

, 2008)Slide50

Septic ArthritisSlide51

PathophysiologyBacterial deposits cause an inflammatory reaction of the synovial membraneSynovium

does not have a basement membrane

Becomes hyperemic and infiltrated with rapidly progressing inflammatory cells

Inflammation develops from acute to chronic within a few weeks

(

Mascioli

& Park, 2013)

Slide52

PathophysiologyInflammatory and infectious cascade that can begin depleting the matrix within 2 days after inoculationHyperplasia develops in 5-7 daysDegradation of the matrix appears within 4-6 days resulting in destruction of articular cartilage

The

articular

cartilage can have complete destruction in approximately 4 weeks

(Abelson, 2009;

Mascioli

& Park, 2013; Matteson &

Osmon

, 2012)

Slide53

EtiologyHematogenous spread: carried by the bloodstream (e.g. indwelling catheters)Inoculation or direct invasion: trauma, accidents, bites, surgery or adjacent infection invading the joint (e.g. osteomyelitis)

Rarely inoculation from arthroscopy or

arthrocentesis

(Abelson, 2009; Matteson &

Osmon

, 2012)

Slide54

Etiology

(

Kherani

&

Shojania

, 2007, p. 1606)Slide55

Causative OrganismsStaphylococcus aureus Most common cause of infection Contain collagen receptors, which are thought to contribute to the infection of the joints

Expression of adhesions, microbial surface proteins, help form

biofilms

that coat prostheses and make effective treatment more difficult

Increase expression of protein A, which interferes with the host immune

opsonization

and

phagocytosis

Group A streptococcus

Enterobacter

(

Mascioli

& Park, 2013;

Raukar

& Zink, 2014) Slide56

Causative OrganismsNeisseria gonorrhoeae Cause of about 75% in healthy, sexually active young adultsAlthough septic arthritis develops in only 3% of those infected with

N.

gonorrhoeae

Presents differently

often

polyarticular

and may have

papular

rash

joint cultures are usually negative, however cultures from pharynx or urethra may be positive

Polymerase chain reaction (PCR) may be helpful

(

Mascioli

& Park, 2013)Slide57

Causative OrganismsHaemophilus influenza was a common cause for children, but has declined drastically since the use of H. influenza b vaccineDecreased by 70-80%

Other:

Mycobacteria

and fungi

Gram-negative bacilli often in neonates, elderly, &

immunocompromised

patients

(Abelson, 2009)

Slide58

Causative OrganismsKingella kingae may be more common than originally thoughtDifficult to recover on solid media by joint cultureSalmonella

Increased likelihood in Systemic lupus

erythematosus

Pseudomonas

In those with history of IVDU

(

Mascioli

& Park, 2013)Slide59

(

Raukar

& Zink, 2014, p. 1834)

Causative OrganismsSlide60

PrevalenceGeneral population: 2-10 per 100,000 (Abelson, 2009)20,000 cases per year in the United States (Cho, Burke, & Lee, 2014)8%-27% present as bacterial acute

monoarthritis

(Cho, Burke, & Lee, 2014)

Rheumatoid arthritis population: 30-70 per 100,000

(Abelson, 2009)

50% of cases involve the knee joint

(Abelson, 2009)Slide61

Risk FactorsDiabetesAlcoholismCirrhosisUremiaCutaneous ulcers

Skin infections

IV drug use

Indwelling IV catheters

RA

OA

Low socioeconomic status

Advanced age

Cancer

Immunosuppressive therapies

Prosthetic joints

Corticosteroid injections Slide62

Charcot Foot

http://trufitusa.com/files/Patient_Education_PICS/patient_ed/CharcotFoot1.png

http://contentwithpictures.com/wp-content/uploads/2013/04/charcot-foot.pngSlide63

Corticosteroid Injections

(Murdoch & McDonald, 2007, p. 2)Slide64

Signs & SymptomsUsually monoarticular but as many as 22% can be polyarticular Hot, swollen, tender joint with decreased range of motion

Fever is an unreliable sign

Chills are uncommon

Symptoms are diminished in the elderly,

immunocompromised

, and IV drug abusers

Symptoms typically less than 2 weeks although can be delayed by low virulence organisms

(Cho, Burke, & Lee, 2014; Mathews, et al., 2008)

Slide65

Signs & SymptomsMore common in large joints60% affecting the hip or knee

About 50% cases involve the knee

Multiple joints occur in 15% of cases

http://www.onmedica.com/getresource.aspx?resourceid=0f058d22-e44f-42cb-8907-b32acf83a1af

(Mathews, et al., 2008)

Slide66

Other Joints InfectedNondiarthrodial joints, are usually associated with IV drug abuse or IV catheters for medical treatments

Symphysis

pubis is associated with prior UTI, pelvic malignancy, IV drug use, or vigorous weight bearing physical activity such as long-distance running in females

(Matteson &

Osmon

, 2012; Google Images, 2014)

Slide67

Physical AssessmentThe joint is held in the position that allow for maximal joint spaceAccommodate for increased fluidIncreased pain with movement

regardless of passive or active ROM

(Cho, Burke, & Lee, 2014)Slide68

Diagnostic Tests Per GuidelinesAspirate synovial fluid:gram stain and culture prior to initiation of antibiotics (anticoagulation therapy is not a contra-indication)Prosthetic joint: always refer to orthopedic surgeonPolarizing microscopy to evaluate crystals in all synovial fluid

(Mathews, et al., 2008)

Slide69

Diagnostic Tests“Neither the absence of organisms on Gram stain, nor a negative subsequent synovial fluid culture, excludes the diagnosis of septic arthritis” (Mathews, et al., 2008, p. 2)Key point: if high clinical suspicion of septic arthritis based on clinical presentation, treat as septic arthritis until proven otherwise!

(Mathews, et al., 2008; Weston &

Coakley

, 2006)Slide70

Additional TestsBlood cultures should always be drawn at the same time as joint aspiration White cell count (WCC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)Again, the absence of elevated WCC, ESR, or CRP does NOT exclude the diagnosisUrea, electrolytes, liver function measurements for detection of end organ damage (a poor prognostic indicator) and renal function tests that may influence antibiotic treatment

Other tests as indicated by H&P: genitourinary, respiratory tract, cervical, urethral, or other infection

(Mathews, et al., 2008)

Slide71

ImagingPlain radiographsno benefit in diagnosis, however does provide baseline for future joint damageScintigraphy and magnetic resonance imaging (MRI): distinguish sepsis from OA but cannot differentiate sepsis and inflammation

not recommended for a hot swollen joint

MRI is preferred for advanced imaging to detect osteomyelitis that may require surgical treatment

Ultrasound or CT may be needed to aspirate septic joints such as the hip

(Mathews, et al., 2008)

Slide72

(Abelson, 2009, p. 1159)

Slide73

(Abelson, 2009, p.

1159; Mathews, et al., 2008)

Recommend joint aspiration to dryness as often as required

Slide74

http://www.dealwitharthritis.com/wp-content/uploads/2013/10/septic-arthritis-treatment.jpegSlide75

Synovial Fluid

(Cho, Burke, & Lee, 2014, p. 497)

(

Kherani

&

Shojania

, 2007, p. 1607Slide76

Differential Diagnoses Crystal-induced arthritis (gout, calcium oxalate, pseudogout, hydroxyapatite crystals)Calcium Pyrophosphate Deposition Disease

Infectious arthritis (bacterial, fungal, mycobacterial, spirochetes, virus)

Rheumatic fever

Inflammatory arthritis (Behcet syndrome, rheumatic arthritis, sarciod, systemic lupus, erythematosus, still disease, seronegative spondyloarthropathy, ankylosing spondylitis, psoriatic arthritis, reactive arthritis, inflammatory bowel disease-related to arthritis, systemic

vasculitis

)

(Horowitz, Katzap, Horowitz, & Barilla-LaBarca, 2011)Slide77

Differential Diagnoses OsteoarthritisAvascular necrosisFractureHemarthrosisHyperlipoproteinemia

Meniscal

tear

Systemic infection (bacterial

endocarditis

, HIV)

Tumor (metastasis, pigmented

villonodular

synovitis

)

(Horowitz, Katzap, Horowitz, & Barilla-LaBarca, 2011)Slide78

Nongonococcal Arthritis TreatmentNongonococcal arthritisGram-positive Cocci80% of patients, primarily older adults

Acute in nature

Synovial fluid are 90% positive

Blood cultures are only positive 50%

Staphylococcus

aureus

40% and streptococcus 28% most identified GPO

Typically associated with IVDU,

cellulitis

, abscesses,

endocarditis

, and chronic

osteomyelitis

(Horowitz, Katzap, Horowitz, & Barilla-LaBarca, 2011)Slide79

Nongonococcal Arthritis Treatment MRSACA-MRSA is emerging, ranges between 5-25% of bacterial infectionsTend to affect older people, primarily shoulder jointsGram-negative bacilliCausative organisms pseudomonas aeruginosa

and E. coli

14% to 19% of septic arthritis patients

Mostly related to invasive urinary tract infections, IVDU, older population,

immunocompromised

patients, and skin conditions

(Horowitz,

Katzap

, Horowitz, & Barilla-

LaBarca

, 2011; Mathews et al., 2008) Slide80

Nongonococcal Arthritis TreatmentRecommended IV antibiotic therapy for Gram-positive and negative cocci:Vancomycin 15mg/kg IV every 12 hours and ceftriaxone 1 gm IV every 24 hours are good initial treatment

If pseudomonas is suspected,

Cefepime

2 gm is given in place of

ceftriaxone

Treatment for

Nongonococcal

infections, IV antibiotic therapy for at least two weeks, followed by one to two weeks of oral antibiotics, tailored to the patent response

(Horowitz,

Katzap

, Horowitz, & Barilla-

LaBarca

, 2011; Mathews et al., 2008) Slide81

Gonococcal Arthritis TreatmentDisseminated neisseria gonorrhoeae

Young, healthy, sexually active adults

Various clinical musculoskeletal clinical presentation, with or without associated skin conditions

25-70% of blood cultures positive, when compared

Nongonococcal

infections

If

Gonococcal

infections are suspected, cultures should be taken from infected source (urethra, rectum, cervix, pharynx)

PCR test has a high specificity 96%, this may be beneficial in culture negative patients, but present with a septic arthritis picture

(Horowitz,

Katzap

, Horowitz, & Barilla-

LaBarca

, 2011; Mathews et al., 2008) Slide82

Gonococcal Arthritis TreatmentTreatment of Gonococcal arthritisIV antibiotics for one to three days, third-generation cephalosporin (usually ceftriaxone 1-2 gm daily)

If the patient responds well, IV therapy can be switched to oral antimicrobial therapy for seven to 14 days

Cefixime

400 mg

po

BID or amoxicillin 500 to 850 mg

po

BID

Doxycycline

and or

azithromycin

can be considered if the patient is positive for

chlamydia

(Horowitz,

Katzap

, Horowitz, & Barilla-

LaBarca

, 2011; Mathews et al., 2008) Slide83

Other Types of Exposure to Septic Arthritis

http://www.aafp.org/afp/2011/0915/p653.pdfSlide84

Pathogen Specific History and Organisms

(https://www.med.unc.edu/tarc/events/event-files/septic%20arthritis%20management.pdf)Slide85

Other Types of TreatmentTreatment of fungal arthritis includes an azole or parental amphotericin B six to 12 weeks (Brusch, 2014)Lyme arthritis responds well to ceftriaxone IV or oral doxycyclineRepeat of joint aspiration is successful during the first five days of treatment to monitor WBC count, polymorphonuclear cell count, Gram stain, and cultures

Arthroscopic drainage increases outcomes and reduces morbidity

Consult Rheumatologist or Orthopedic surgeon

(Horowitz,

Katzap

, Horowitz, & Barilla-

LaBarca

, 2011; Mathews et al., 2008) Slide86

Treatment Algorithm

https://www.med.unc.edu/tarc/events/event-files/septic%20arthritis%20management.pdfSlide87

Health Promotion/ PreventionInform your doctor and dentist about a prosthetic joint prior to any type of procedure

Educate the patient of signs of infections

HIV

or immunocompromised patients require a therapeutic relationship with their PCP to discuss antibiotics prior to a

procedure, regular

visits to monitor for joint or

skin

infections, and any slow healing cuts or sores.

Up to date vaccinations

Traveling

out of the country or to another state; you may

be exposed to different insects or require vaccinations

(CDC, 2014)Slide88

Health Promotion/PreventionIVDU- this is the most common way to introduce a foreign bacteria into your body, which can lead to infective arthritis. IVDU are at higher risk for developing recurrent joint infections. Bacteremia can increase the risk for infective

arthritis

Weight management and balanced diet

Practice safe sex, use protection

Ensure patients have access and availability to evidenced-based arthritis interventions addressing basic information, weight management, injury prevention, and physical activity tips

(CDC, 2014)Slide89

Outcomes for Septic ArthritisMortality rates ranges 10-20%, depending upon comorbiditiesGreater than 65 years or older and infection in shoulder, elbow, or multiple sites are factors associated with increased mortality

Pneumococcal septic arthritis patients mortality rates ~ 20%, but regain almost full function of their joint

S. aureus causative agents only regain 46-50% of their baseline joint function upon completion of antimicrobial therapy

(

Shirtliff

&

Mader

, 2002; Horowitz,

Katzap

, Horowitz, & Barilla-

LaBarca

, 2011)Slide90

Outcomes for Septic ArthritisThe high rate has not changed significantly over the past 40 years due to the difficultness of the diagnosis

Treatment initiated after seven days or more demonstrate a worse outcome

Prompt diagnosis and initiation of empiric antimicrobial therapy is utmost importance to improve quality of life and outcomes

Early involvement in therapy and aggressive movement of the joint increases optimal outcomes

An

extended time > 6 days required to sterilize the joint is another indicator of poor

prognosis

(

Shirtliff

&

Mader

, 2002)Slide91

Follow-up Follow-up appointments are pertinent to maintain to monitor for improved or worsening of the jointLaboratory data will be monitored weekly for adverse reactions secondary to IV antibiotics (CBC, BMP, LFT’s, CRP, ESR)

Most Patients will have an indwelling PICC line, which increases an individuals risk for bacteremia, close monitoring of site and presence of cord

Discuss any questions or concerns with your ACNP to ensure understanding of the diseaseSlide92

Question #1 All of the following regarding OA are true EXCEPT:A: Evidence of bilateral swelling and warmth affecting only the wristsB: Joint space narrowing and

osteophytes

at the proximal and distal

interphalangeal

joints on x-ray

C: Pain that becomes worse when preparing meals

D: Stiffness that is worse after brief periods of rest with occasional locking of the more affected joints Slide93

Question #1 AnswerA: Evidence of bilateral swelling and warmth affecting only the wristsJoints of the hands are most commonly affected, but the wrist is uncommon OA can also occur in the hips, knees, cervical and

lumbosacral

spine

Pain occurs with joint use and relieves with rest

Joint stiffness usually occurs after periods of restSlide94

Question #2 47 y.o. female presents complaining of pain in her hands in the mornings. She drops things and feels she has difficulty maintaining her grip. X-ray reveals bilateral soft tissue swelling of her metacarpals. The ACNP knows additional testing findings will include:

A: Rheumatoid Factor (RF) +

B:

Heberden’s

nodes +

C: Anti-CCP Antibodies +

D: Antinuclear antibody (ANA +) Slide95

Question #2 AnswerC: Anti-CCP AntibodiesAnti-CCP has a higher sensitivity than RF, and is more likely to be positive early in disease.

Heberden’s

nodes are present in osteoarthritis.

ANA is not positive in RA.Slide96

Question #3Which of the follow statements is NOT true regarding RA?

A: RA results in joint degeneration, which causes deterioration of bone formation at the joint surfaces.

B: Patients with RA have on average an onset of cardiovascular disease 10 years earlier than those without RA

C: Morning stiffness and joint pain are characteristic symptoms

D: RA is a chronic inflammatory disease of the synovial joint and tendon sheath Slide97

Question #3 AnswerA: RA results in joint degeneration, which causes deterioration of bone formation at the joint surfaces.Joint degeneration is consistent with osteoarthritis, not RA.Slide98

Question #466 y.o. with a history of RA and pseudogout presents with night sweats and a 2-day history of left knee pain. Temp is 101.5. WBC is 16,000. Tap of knee shows 168,000

WBCs

, 99%

neutrophils

and crystals. Gram stain shows gram +

cocci

.

Management for this patient includes all of the following EXCECPT:

A: Blood cultures

B:

Glucocorticoids

C: Needle aspiration of joint fluid

D: Orthopedic surgery consult

E:

Vancomycin

Slide99

Question #4 AnswerB: GlucocorticoidsCrystals are suggestive of active pseudogout

Septic arthritis (SA) is the patient’s major problem with a joint leukocyte count >100,000 and a positive gram stain.

SA should be treated aggressively with antibiotics, a surgical consult should be completed for possible joint drainage and cultures should be sent to assess for

bacteremia

. Slide100

Question #524 y.o. admitted with fever, swollen and painful right knee. 3 weeks earlier she had systemic symptoms: fever, chills and migratory joint pains. Rash over her chest and hands. She has no significant history. Clean arthrocentesis

.

A: Bacterial cultures of the cervix

B: Bacterial cultures of the synovial fluid

C: Blood cultures

D: Rheumatoid factor

Slide101

Question #5 AnswerA: Bacterial cultures of the cervixThe patient’s history is consistent with septic arthritis due to a gonococcal infection.

Diagnostic procedure is to culture the infected mucosal site, including the cervix, urethra or pharynx.

Neisseria

gonorrhoeae

is responsible for about 70% of acute arthritis infections in patients younger than 40.

Patients usually present with fever, chills, migratory

arthralgias

and a rash 3 weeks prior to

monoarticular

septic arthritis. Slide102

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