Upload
joshua-french
View
241
Download
0
Embed Size (px)
Citation preview
NON-GONOCOCCALSEPTIC ARTHRITIS
Outline
Introduction Risk Factors Pathogenesis Microbiology Clinical Features Treatment Prognosis Special Cases
2
Introduction
Infectious arthritides Non-gonococcal septic arthritis Gonococcal arthritis Lyme disease Viral arthritis Fungal arthritis Osteomyelitis
Bacterial joint infection are serious Most rapidly destructive form of acute arthritis Significant mortality (10-15%) and morbidity (25-50%) Irreversible loss of function in up to 50% of patients
Hochberg et al. Chapter 96. Copyright ©2008 Elsevier Inc.
3
Septic Arthritis
Incidence 2-6/100,000 in general population 30-60/100,000 in patients with RA and/or joint prostheses
Despite advances over last 25 years, fatality rate unchanged Although decreased number of prosthetic joint infections,
prosthetic joints remain most common cause of joint infections
Most important prognostic indicator Speed of diagnosis and treatment
General rule If treated within 7 days, patients generally do well
Hochberg et al. Chapter 104. Copyright ©2010- Elsevier Inc.
4
Risk Factors for Septic Arthritis Recent joint surgery (+LR 6.9, 95% CI 3.8-12.0) Age > 80 years (+ LR 3.5, 95% CI 1.8-7.0) Prosthetic joint (+LR 3.1, 95% CI 2.0-4.9) Skin infection (+LR 2.8, 95% CI 1.7-4.5) Diabetes mellitus (+LR 2.7, 95% CI 1.0-6.9) Preexisting RA (+LR 2.5, 95% CI 2.0-3.1) TNF-I (?) Others Impaired immune system (cirrhosis, malignancy) Renal failure and hemodialysis Hemophilia Indwelling catheters IVDA & alcoholism
Margaretten ME, et al. JAMA 2007; 297(13):1478-1488.
5
Pathogenesis
70%
20%
Arthrocentesis or Arthroscopy
Hochberg et al. Figure 96.1. Copyright ©2008 Elsevier Inc.Gilliland, WR. Rheumatology Secrets, 2nd ed, ed. West 2002. Hanley & Belfus: Philadelpha, pp. 281-289.
6
Pathogenesis
Bacteria enter joint, deposit on synovial membrane Produce inflammatory response
Synovial tissue proliferates, becomes tender, blood flow increases Exudation of bacteria, cells, and proteins into SF
No limiting basement membrane Within 5-7 days
Joint becomes swollen Elastase, collagenase liberated from PMNs, synovial cells
degrade cartilage Infection, inflammation can spread to subchondral bone Pressure necrosis from large effusions result in further cartilage
and bone loss
8
Pathogenesis
Bacterial DNA and toxins may have deleterious effect Staphylococcal toxic shock syndrome toxin (TSST)-1 Staphylococcal enterotoxins
Adhesins on bacteria probably important (MSCRAMMs) Important virulence factor Mediate adherence of bacteria to intraarticular proteins
Fibronectin, laminin, elastin, collagen, hyaluronic acid, and to prosthetic joint materials
Likely why S. aureus causes most septic arthritis
Hochberg et al. Chapter 96. Copyright ©2008 Elsevier Inc.
9
Pathogenesis10
Microbiology
Gram-positive cocci (75-80%) S. aureus most common in native and prosthetic joints
Most common etiologic agent in 40-70% of cases Increasing incidence of CA-MRSA
Streptococci S. epidermidis common in prosthetic joints, rare in native joints
Gram-negative bacilli (10-20%) Elderly who are predisposed to systemic GNR infections Immunocompromised (e.g. SLE patients)
Anaerobes (1%) Occur in prosthetic joints, rare in native joints
Gilliland, WR. Rheumatology Secrets, 2nd ed, ed. West 2002. Hanley & Belfus: Philadelpha, pp. 281-289.Hochberg et al. Chapter 96. Copyright ©2008 Elsevier Inc.
11
Microbiology of Septic Arthritis
Organism Clinical Clues
Staphylococcus aureus Healthy adults, skin breakdown, previously damaged joint (e.g. RA), prosthetic joint
Streptococcal species Healthy adults, splenic dysfunction/asplenia
Neisseria gonorrhea Healthy adults (particularly young, sexually active), F >> M’s, associated tenosynovitis, vesicular pustules, late complement deficiency, negative SF culture and gram stain
Aerobic gram negative bacteria Immunocompromised hosts, GI infection
Anaerobic gram negative bacteria Immunocompromised hosts, GI infection
Mycobacterial species Immunocompromised host, recent travel to or residence in an endemic area
Fungal species (sporotrichosis, cryptococcus, blastomycosis)
Immunocompromised host
Spirochete (Borellia burgdorferi) Exposure to ticks, antecedent rash, knee joint involvement
Mycoplasma hominis Immunocompromised hosts with prior GI tract manipulation
UpToDate®
12
Joint Distribution
Monoarticular (80-90%) Predilection for single large joint, typically the knee or hip (60%) LE >> UE (particularly the knee) Always consider septic arthritis in DDx of an acute monoarthritis
Polyarticular (10-20%) More common in those with preexisting arthritis S. aureus is the major pathogen May portend a less favorable outcome
>50% mortality rate in RA patients Aspirate >1 joint when suspected
13
Clinical Features of Septic Arthritis
Joint capsule Tumor (78%), Rubor, Calor
Severe pain (Dolor) (85%) Typically abrupt onset
Fever (57%) Sweats (27%) Rigors (19%)
Inflammatory SF Leukocytosis (45%) Elevated CRP/ESR (87%)
14
Margaretten, ME, et al. JAMA 2007; 297(13):1478-1488.
Diagnosis (no gold standard) Traditional ‘index of suspicion’
Positive Gram stain OR
Positive cultureOR
Positive synovial biopsy or PCROR
Typical clinical syndrome with response to Rx
15
Arthrocentesis –Cornerstone of Diagnosis
Cell Count Progressively higher SF WBC increases likelihood
< 25,000/μL (+LR 0.32, 95% CI 0.23-0.43) ≥ 25,000/μL (+LR 2.9, 95% CI 2.5-3.4) > 50,000/μL (+LR 7.7, 95% CI 5.7-11.0) > 100,000/μL (+LR 28.0, 95% CI, 12.0-66.0)
Wide range depending on timing, abx pre-treatment, etc. Typically a preponderance of PMNs
≥ 90% (+LR 3.4, 95% CI, 2.8-4.2) <90% (+LR 0.34, 95% CI, 0.25-0.47)
16
Margaretten, ME, et al. JAMA 2007; 297(13):1478-1488.
Arthrocentesis –Cornerstone of Diagnosis
Gram stain (+ in 50-80%) Wet prep examination for crystals Culture (+ in majority of NG septic arthritis)
False (-) due to fastidious organisms or recent antibiotics Blood culture bottles reduces the false (-) results
Inoculation of bottles should be done in the lab, not at bedside Synovial glucose, protein, and LDH not helpful
Blood cx’s may id causative agent when SF cx unrewarding
17
Matthews, CJ et al. Ann Rheum Dis 2007; 66:440-445.UpToDate®
UpToDate®
18
Pseudoseptic Arthritis
First described in 1985 by Call et al. Acute arthritis (mono-/oligo-) superimposed on
chronic rheumatic disease with associated fever, inflammatory SF, and (-) culture
RA Gout Apatite-related arthropathy PsA Dialysis-related amyloidosis Plant thorn synovitis PVNS Neuropathic arthropathy
JIA Pseudogout ReA SLE Sickle cell disease Transient osteoporosis synovitis of the hip Metastatic carcinoma Hemarthrosis
19
Imaging Adjuncts to Diagnosis
Plain films Presence of radiographic changes indicates that infection has
been present for 2-3 weeks or more Sonography
Useful for diagnosis of effusions, ST fluid collections Not useful for evaluating the presence of osseous infection
CT Detect early osseous erosion, sequestrum, foreign body,
gas formation Less sensitive than MRI/scintigraphy for detection of bone
infection
20
Scintigraphy
Useful in identifying multifocal involvement
Hochberg et al. Chapter 96. Copyright ©2008 Elsevier Inc.
21
MRI with Gadolinium
Synovial enhancement in 98% Due to increased vascularity Associated with perisynovial edema (84%), synovial thickening (22%)
Joint effusions common (70%) 91% of large joints, 54% of small joints Absence of effusions in not an absolute (-) predictor
Abnormal bone marrow signal has highest association with concomitant osteomyelitis Especially if diffuse and on T1-weighted images But also had a high false (-) rate
Karchevsky M, et al. AJR 2004; 182:119-122.
22
Radiologic and Pathologic Changes(A-B-C-D-E-S)
Radiographic Sign Pathologic Correlate
A Bony ankylosis Fibrous or bony ankylosis (end-stage)
B Osteoporosis Increased blood flow, inflammatory cytokines
C Joint space loss Pannus with cartilage destruction
D Joint deformity End stage of arthritic destruction
E Erosions Pannus with bony destruction
S Joint effusion (the first sign), soft-tissue swelling
Edema of synovium with fluid production
Gilliland, WR. Rheumatology Secrets, 2nd ed, ed. West 2002. Hanley & Belfus: Philadelpha, pp. 281-289.
23
Therapy for Septic Arthritis
Prompt treatment ! Start antibiotic(s) immediately after samples collected Use Gram stain and clinical scenario to make choice Broad coverage in debilitated elderly if Gm stain inconclusive
Once organism identified and sensitivities known Continue with
Most efficacious agent With best safety profile And lowest cost
24
Therapy (no RCTs)Gram Stain Results Antibiotic
Gram-positive Cocci Vancomycin (30 mg/kg daily IV in 2 divided doses not to exceed 2 gm per day unless serum levels monitored)
Gram-negative Bacilli
If cephalosporin allergy
If suspect Pseudomonas
3rd generation cephalosporin Ceftazidime 1-2 gm IV q8h OR Cetriaxone 2 gm IV q24h OR Cefotaxime 2 gm IV q8h
Ciprofloxacin 400 mg IV q12h OR 500-750 mg PO q12h
Add Gentimicin 3-5 mg/kg/day in 2-3 divided doses
Negative Gram Stain
Immunocompetent
Immunocompromised or traumatic arthritis
Vancomycin
Vancomycin plus 3rd generation cephalosporin
UpToDate®2008.
25
Therapy (no RCTs)SF Gram-Stain Findings Initial Antibiotic Regimen
Gram-positive
Gram-positive cocci in clusters (presumptive Staphylococcus)
Gram-positive cocci in chains (presumptive Streptococcus)
Nafcillin or oxacillin(add aminoglycoside if IVDA)
Nafcillin or oxacillin
Gram-negative
Gram-negative bacilli
Gram-negative diplococci (presumptive gonococcus)‡
Nafcillin or oxacillin/aminoglycoside†
Ceftriaxone or cefotaxime
†All with prosthetic joints, IV’s, or recent hospitalization are at risk for MRSA infection and should receive Vanc until cx results available, regardless of Gram-stain results.
‡In the absence of definitive Gram-stain results, a reasonable empiric regimen for the adult with possible septic arthritis is the combination of naf-/oxacillin with a cephalosporin (3 rd- or 4th-generation). An AMG should be added in IVDA. Vanc should be substituted for nafcillin/oxacillin if MRSA is a possibility.
Ho, G Jr. Septic Arthritis. Primer on the Rheumatic Diseases, 3rd ed, ed. Klippel. Springer: NY, 2008. Pages 271-276.
26
How Long to Treat? It Depends…
Clinical Scenario Duration of Treatment
Uncomplicated native joint infections 2-4 weeks IV, then 2-3 weeks PO
Difficult to treat pathogens 3-4 weeks IV
Serious infection in compromised host 4-6 weeks IV
Bacteremia with secondary arthritis 4 weeks IV
Prosthetic joint infections Protracted course
27
Therapy (no RCTs)
Drainage of purulent material Goals:
Relieve pain Eradicate infection Hasten recovery of lost function
Can be done surgically or via closed needle aspiration Controversy over which should be employed Only one paper compares the two
Retrospective analysis with small number of cases Results suggested needle aspiration appeared, in general, to be
preferable as the initial mode of treatment, but results did not have statistical significance
28
Matthews, CJ et. Ann Rheum Dis 2007; 66:440-445.
Therapy (no RCTs)
Overall recommendation is to involve Orthopedics To help facilitate best choice of drainage procedure Arthroscopy often preferred for knee and shoulder Initial open drainage may be necessary for hip
Immobilization of affected joint initially
PT/OT as soon as patient can tolerate
Effective analgesic medication
NSAIDs for post-infectious synovitis
29
When is Surgical Drainage Necessary?
Infected hip joints, probably shoulder joints Vertebral osteomyelitis with cord compression Needle aspiration technically difficult Inability to remove purulent fluid by needle drainage Sterilization of the joint fluid is delayed (>7 d) Joint already damaged by preexisting arthritis Associated osteomyelitis requiring surgical debridement Arthritis associated with foreign body
Gilliland, WR. Rheumatology Secrets, 2nd ed, ed. West 2002. Hanley & Belfus: Philadelpha, pp. 281-289.
30
UpToDate®
Diagnostic approach to suspected bacterial arthritis
31
Prognosis
Morbidity 30%, Mortality 10-15%* Factors portending poor outcome
Young age, old age Virulent microorganisms Delay in diagnosis/treatment Presence of underlying joint disease (e.g. RA) or prosthetic joint Infection of particular joints (shoulder, hip) Polyarticular* Positive blood cultures* Comorbid conditions (RA, IS, renal or cardiac disease)*
Carola, J et al. Arthritis Rheum 1997; 40(5): 884-892.Ho, G Jr. J Rheum 1993; 20: 2001-2003.
32
Why Worse Prognosis in RA?
Previously damaged joints Immunosuppression Steroids may blunt symptoms
May be mistaken for a “flare” of RA Gram positive organisms (75-90% of infections)
Mortality 25% Only 50% surviving attain pre-infection level of function
33
Prosthetic Joint Infections
Infection rate Knee 0.8-1.9% Hip 0.3-1.7%
Extremely costly Clinical Features
Depend on timing Early (< 3 months) Intermediate (3-24 months) Late (>24 months)
34
Prosthetic Joint Infections35
Del Pozo JL, N Engl J Med 2009; 361(8):787-794
Risk Factors for Prosthetic Joint InfectionsEarly Infection Late Infection Signs of Infection
Prolonged duration of surgery Type of prosthesis Slow recovery
Number of OR personnel RA Wound infection
Inexperienced primary surgeon
Nonarticular infections UTI
Advanced age Duration of implant(?) Failed fracture
RA Loosening of implant (?) Increased pain
Periop nonarticular infections Decreased ROM Diabetes
• Revision arthroplasty has a 5-10x increased risk!
From UpToDate®. Adapted from Wymenga, et al., Acta Orthop Scand 1992; 63:665,and from Blackburn, WD Jr, Alarcon, GS, Arthritis Rheum 1991; 34:110.
36
Pathogenesis of Prosthetic Joint Infections Wound contamination Hematogenous seeding Microbiology
Early infections typically due to S. epidermidis Late infections (hematogenous) due to S. aureus > others
Mucoid biofilm Coalesced glycocalyx forms on prosthetic joint Protective environment from host defenses, antimicrobials
37
Diagnosis
Joint fluid analysis is key Leukocytosis (<10%) Fever (<50%) Elevated ESR/CRP Cultures or tissue biopsy Radiographs Scintigraphy
Gallium or technetium scans DDx includes aseptic joint loosening
38
Treatment of Infected Prosthetic Joints
Surgical removal of hardware > 90% of prosthesis have to be removed
Arthrodesis Antibiotics
5-6 weeks of IV antibiotics Rifampin used in conjunction with other antibiotics
Delayed implantation with antibiotic impregnated cement Reinfection rate 10% at 3 yrs, 26% at 10 yrs Mortality 5-20%
39
40
Prevention of Septic Arthritis
Antibiotic prophylaxis for dental procedures in patients who have undergone total joint replacements Within 2 years of implant Immunocompromised patients Patients with certain comorbidities
Controversial with no supporting studies; only consensus statements (2003)
Risk of late infection low 10-100 cases per 100,000 patients per year Counsel your patients
41
Prevention of Septic Arthritis
42
J Am Dent Assoc 2003; 134(7):895-899
Prevention of Septic Arthritis
43
J Am Dent Assoc 2003; 134(7):895-899
Summary
Septic arthritis is the most potentially dangerous and destructive forms of arthritis
Risk factors include age > 80, DM, RA, prosthetic joints, recent joint surgery, and skin infection
Most common etiologic microorganism is S. aureus Don’t forget CA-MRSA, HA-MRSA!
Cornerstone of diagnosis is arthrocentesis Key to better prognosis is to treat ASAP Significant morbidity and mortality
44
From UpToDate®. Adapted from Wymenga, et al., Acta Orthop Scand 1992; 63:665,and from Blackburn, WD Jr, Alarcon, GS, Arthritis Rheum 1991; 34:110.
Special Cases45
Septic Arthritis in Children
>90% monoarticular Knee and hip in 2/3 of cases Children <2 years old more susceptible
Signs of joint disease in neonate/infant minimal/absent S. aureus > Grp B strep, Gram negatives
Decline in H. flu septic arthritis in kids < 5 Septic arthritis often secondary to adjacent osteomyelitis
Metaphyseal and epiphyseal blood vessels communicate Some long bone metaphyses are within joint capsule
46
Septic Arthritis in Children
Age very helpful in determining likely organism
Age Microorganism
Neonates Staphylococcus aureus (hospital-acquired)Streptococci (community-acquired)Gram-negative bacilli
Age < 2 years Haemophilus influenzae (less common with immunizations)Staphylococcus aureus
Age 2-15 years Staphylococcus aureusStreptococcus pyogenes
Gilliland, WR. Rheumatology Secrets, 2nd ed, ed. West 2002. Hanley & Belfus: Philadelpha, pp. 281-289
47
Septic Arthritis (SA) in Children
AVN of femoral head can complicate SA of the hip Outcome more favorable than in adults Long-term sequelae occur in 25% of cases
Leg length discreptancy Limitation of joint mobility Secondary degenerative joint disease
48
IVDA and Septic Arthritis
Clinical signs and symptoms may be subtle Common sites – axial skeleton
Sternoclavicular joint Sternomanubrial joint Lumbar vertebrae SI joint, symphysis pubis
Organisms Staphylococcus aureus Staphylococcal epidermidis GNRs (Pseudomonas, Serratia) Candida spp.
Good prognosis if given proper therapy unless HIV +
49
More Special Populations
Underlying Disorder Microorganisms
Alcoholism/cirrhosis Gram negative bacilli, Streptococcus pneumoniae
Malignancies Gram negative bacilli
Diabetes mellitus Gram negative bacilli, Gram-positive cocci
Dog/cat bites Pasteurella multocida
Hemoglobinopathies Streptococcus pneumoniae, Salmonella spp
Raw milk/dairy products Brucella spp
SLE Encapsulated organisms (Neisseria, Salmonella, Proteus)
Gilliland, WR. Rheumatology Secrets, 2nd ed, ed. West 2002. Hanley & Belfus: Philadelpha, pp. 281-289
50
Septic Bursitis
UpToDate® (above)Hochberg. Figure 96.4. (left)
51
Septic Bursitis
Superficial bursae more susceptible to infection Olecranon bursa, prepatellar bursa (“housemaid’s knee”)
Etiology is direct extension of superficial infection Extensive cellulitis surrounding bursa (>50%) Look for skin lesions which are portal of entry Can also see distal edema of affected limb
Cause typically due to trauma to superficial bursae Carpet laying, mining, plumbing, roofing, gardening,
wrestling, gymnastics, hemodialysis
52
Septic Bursitis Management
Aspirate effusion/fluctuance Fluid usually inflammatory
WBC elevated but not as much as septic joints Use large bore needle if fluid thick Gram stain usually positive for gram positive cocci
Start bactericidal anti-staphylococcal agent S. aureus responsible for >80% of cases
53
Septic Bursitis Management
Mild infection Oral agent Outpatient follow-up and adequate drainage
Severe infection Admission and serial aspirations Parental antibiotics Oral abx after control of infection for additonal 1-3 wks
Surgical drainage or bursectomy rarely necessary Prognosis excellent
54
Mycobacterium Infections
Tuberculosis Osteoarticular involvement in 1-5% Infection via hematogenous spread Types of articular infections
Spinal tuberculosis Peripheral joints Reactive
55
Pott’s Disease
Tuberculous spondylitis Most common form of osteoarticular infection Thoracic > lumbar > cervical > sacral Collapse of anterior vertebral body
Gibbus deformity May extend
Adjoining discs, vertebrae, distant sites Paravertebral or psoas abscesses
56
57
Above: Gibbus deformityLeft: Paravertebral abscess
Tuberculosis Joint Infections
Peripheral arthritis Monoarticular (hips, knees) Insidious, limited inflammation Phemister’s triad
Juxta-articular osteopenia Marginal erosions Gradual narrowing of joint space
SF WBC increased AFB smears (20% +) Cultures (80% +) Diagnosis best made by
synovium biopsy
58
Mycobacterium Infections
Reactive Arthritis AKA Poncet’s disease Polyarticular arthritis in
setting of active TB Hands and feet SF, synovium sterile Resolves with TB
treatment
Others BCG vaccine
May cause a reactive arthritis as well
Atypical mycobacteria M. marinum M. kansasii M. avium complex
M. leprae
59
Fungal Infections
Candida Rare C. albicans
Coccidiomycosis Primary Disseminated Polyarticular Migratory Chronic knee
monoarthritis
Sporotrichosis Blastomycosis Cryptococcosis Histoplasmosis Actinomyces Aspergillus
May mimic Pott’s dz Parasites
Giardia, entamoeba, trichomona, toxoplasma
60
Questions?61