Transcript Septic arthritiis &post arthroplasty infections

Septic arthritis
&post
arthroplasty
infections
Presenter R N MBUVA
Moderator Mr MWANGI
scope
• Septic arthritis
• Prosthetic infections
•Part 1
•Septic arthritis
Definition
• Inflammation of a synovial membrane with purulent
effusion into the joint capsule, often due to
bacterial infection
Synonyms
• Bacterial, suppurative, purulent or infectious arthritis,
gonococcal or nongonococcal
septic arthritis
• 0.2%-0.7% of hospital admissions
• Peak incidence in the first years of 1st decade and
>50 years
• Males>Females
Risk Factors for Septic
Arthritis
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Previous arthritis
Trauma
Diabetes Mellitus
Immunosupression
Bacteremia
Sickle cell anemia
Prosthetic joint
Infection Sources
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Trauma: direct
Hematogenous: IV drug injection
Osteomyelitis adjacent to joint capsule
Soft tissue infections: cellulitis, abscess, bursitis,
tenosynovitis
Pathogenesis
• Systemic bacteremia-invades synovial cartilage
• Postulation-collagen receptors in staph aureus
-lack of basement membrane in
capillaries of synovium
-synovial fibroblasts inhibit phagocytosis
pathogenesis
• Features of acute Infiltration
• Lymphocytes 3/52
• Destruction of cartilage after ground substance
degradation4-6/7
• Depletion of ground substance-activation of
bacteria enzymes and T lymphocytes
• Ground substance degradation-collagen exposed
Up-to-Date 2004
clinical presentation
• Painful ROM, swelling, erythema, not
bearing weight, recent illnesses
• Children:
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pseudoparalysis or disuse of limb, not septic
antalgic limp
Fevers not consistent
Have parent examine the child
Labs
• Leukocyte count not reliable early stages
o 25% of children had elevated counts and 65% the diff was
abnormal
• ESR
o Nonspecific test of inflammation
o Affected by cell size, shape and protein content
• i.e. sickle cell, anemia, steroids
o Not reliable in neonates
o Elevated in 48-72 hrs returns to baseline 2-4 weeks
Mayo series, Morey et al:
only 5 of 76 had ESR below 20mm/hr,
elevated in 90% of patients w/ septic arthritis
ESR
• No change w/ antibiotic therapy
• Continues to rise 3-5 days – after this may consider
change in tx
• Not good for early evaluation of tx
CRP
• Rises within 6 hrs and peaks 30-50hrs
• Half life 47hrs
• Makes this marker of greater value for early
diagnosis and resolution of inflammation
• CRP is elevated in trauma, in otitis
media(22%bacterial 65% viral)
• Blood cultures
Cultures
o yield organisms 30-50% of cases
o Decreases w/ previous antibiotic therapy
• Aspiration of joint fluid
o Gram stain, leukocyte cell count, PMNs
• Cell counts 80,000 – 100,000/ml likely septic arthritis
o Frank and Nelson: 126 positive culture
• Counts of 50,000/ml or less in 55%, 34% had <25,000/ml, only
44% had >=100,000/ml
• Other inflammatory processes can give you >80,000/ml
• Gram stain can give you a presumptive early
diagnosis
o 1/3 are positive
Imaging
• Plain x rays
• Ultrasound
o Used frequently in pediatrics assessing the hip for
effusion/dislocations
o Cannot differentiate between TSH and septic arthritis
by positive effusion alone
o If extracapsular effusion may distinguish between
osteomyelitis around hip/pelvis
• CT,MRI&Bone scans not necessary
• Bone scan – Tc99-good osteoblastic activity
indium111 and gallium citrate more sensitive
and specific
for infection
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• CT scans-good anat,distinguishes soft tissue and
bone infection
• MRI sensitivity 97% and specificity 92%
Kocher et al. 1999
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Hx of fever
Nonweightbearing
ESR >40mm/hr
WBC >12,000/mm3
Kochers criteria
• The likelihood of septic arthritis was
• 0.2% if no criteria were present,
• 3% if one
• 40% if two
• 93% if three
• 99% if four
• Unfortunately not reproducible
• Caird et al-crp&esr –more likely
• Luhmann-visit another facility more likely
Management
• Nade
• Principles-1joint adequately drained
2ABX given to diminish effects of
sepsis
3joint rested in a stable position
Indications for Surgery
Aspiration vs. debridement
Joint does not respond to serial aspirations
No improvement in 48hrs of tx
Frank pus is aspirated
Loculations noted on MRI or U/S
Documented Hip and SI septic arthritis
should be debrided surgically
• No change in morbidity between
arthroscopic vs. arthrotomy of knee
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Abx Treatment
• IV abx 4-7 days
• Check CRP,WBC every 2 days
• Once labs normalize and clinically improving
consider discharge
• Continue tx 2-3 weeks with oral or IV abx (PICC line)
• No true standardization of tx
• Get ID involved
Rehabilitation
• Splinting for 48 hrs
• Salter 1981
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Rabbit knees septic S. aureus
Had arthrotomy and abx tx
Casting vs. ROM w/ CPM vs. cage activity
CPM fared sig. better on pathology of cartilage w/ decreased ground
substance
• WBAT once rom and pain subsided
Prognosis and
complications
• Poor prognosis factors
o Immunodeficiency, RA, prematurity,
osteomyelitis, hip, prosthetic infections, + blood
cultures, symptoms >1 week, >4 joints, + cultures
after aspiration after 7 days of abx tx
• Complications:
o Mortality 8%-15% in three series
o arthritis stiffness, dislocation, subluxation, AVN,
local growth distrubance, osteomyelitis,
postinfection synovitis
• Favorable outcome in 50%-80% of cases
Lyme Arthritis
• Caused by infection with the spirochete Borrelia
Burgdorferi
• Early stage disease
o Localized - Erythema chronicum migrans, fever, arthralgia
and myalgia, sore throat,
o Disseminated- disseminated skin lesions, facial palsy,
meningitis, radiculoneuropathy, and rarely heart block
o Early disease may remit spontaneously
o 50% of untreated cases develop late features
• Late
o Arthritis is a manifestation of late disease-months or years
after exposure
o Intermittent migratory asymmetric mono- or oligo-arthritis
o 10% develop chronic large joint inflammatory arthritis
Lyme Arthritis
• Treatment
o Early localized
• Doxy 100 mg po BID or Amox 500 TID (kids) for 2-4 weeks
o Early disseminated or late disease
• Oral or parenteral abx depending on the severity of the disease
o Neuro or cardiac disease usually treated with IV ceftriaxone 2 g
daily for 3-4 weeks.
o Lyme arthritis may be treated with oral abx for 4 weeks.
Disseminated gonococcal infection
• Occurs in 1-3% on patients infected with GC
• Most patients have arthritis or arthralgia as a
principal manifestation
• Common cause of acute non-traumatic mono- or
oligo-arthritis in the healthy host
Gonococcal arthritis
Host factors
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Women > men
Recent menstruation
Pregnancy or immediate postpartum state
Complement deficiency (C5-C9)
SLE
Gonococcal arthritis
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Consider screening/treating for chlamydia
HIV testing
Syphillis testing
Screen sexual partners
Gonococcal arthritis
• Ceftriaxone 1gm IV or IM q24 hours
• Spectinomycin 2 gm IV or IM q12 hours for ceph
allergic patients
• May use fluoroquinolones if susceptible
Parvovirus B19 Arthritis
• Small non-enveloped DNA virus
• Erythrovirus genus
o Replicates only in erythrocyte precursors
• Transmission
o Respiratory, parenteral, vertical
• 25-68% of infections are asymptomatic
Erythema Infectiosum
• “5th disease”
• 10% of children and 50%
of adults have joint
symptoms
Parvovirus B19 Arthritis
• Begins about 2 weeks after infection
• Symmetrical involvement of the small joints of the
hands and wrists and the knees
• Usually resolves in about a month without joint
damage
• 20% may have persistent disease**
Parvovirus B19
• Clinical features may mimic an early autoimmune
disease
• High prevalence of autoantibodies
o RF, ANA, ACA, ANCA, anti-ds DNA
o May persist for some time after infection is cleared
• Has been implicated in the pathogenesis in both RA
and SLE
Diagnosis and Therapy
• Parvovirus B19 IgM +
o Parvovirus B19 IgG indicates past infection.
• highly prevalent in the general population since
asymptomatic infxn is very common.
• PCR can be used
o Immuncompromised people may not mount an
antibody response
• Therapy is supportive
o NSAIDs
o Steroids are rarely necessary
Tuberculous arthritis
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History of exposure is helpful
PPD may be negative
Synovial fluid stain usually negative
Culture may take 6-8 weeks to grow
Best yield is probably synovial biopsy
•PART 2
•POST
ARTHROPLASTY
INFECTIONS
INCIDENCE
• For knee generally low 0.1-2%
• For hip 1-2%
MECHANISM
• Intraoperative seeding-low virulent
• Blood spread
• Fretting-micromotion between implants
-DM
-sepsis
-steroid use
-Long hospital stay
-long theatre time>3hrs
-blood loss > 1500cc
-smoking
Methods of prevention
• Treatment of superficial and deep infection
• I.V prophylactic antibiotics
• Others-laminar flow
-closed body exhaust suits
-careful tissue handling
-antibiotic cement
-minimize theatre traffic
BIOFILM
• There are five stages of biofilm development
1Initial attachment-van der waals forces
2Irreversible attachment-cell adhesion structures,
hydrophobicity,quorum sensing
3Maturation I:
4Maturation II:
5Dispersion:
BIOFILM
Biofilm
• Pathophysiology has been greatly improved by the
biofilm model
• Conditions for biofilm formation: necrotic tissue and
bone, which have a foreign-body effect and are
colonized by bacteria.
• Pathogens 1st form surface colonies, multiply.
Biofilm
• Matrix offers protection from mechanical
influences and makes it harder for AB,
body’s own defense cells, and Ig to
penetrate, functioning as a diffusion barrier.
• Pathogens pass from a high metabolic rate
and rapid multiplication into greatly
reduced metabolism and slowed biological
Rx.
• This can reduce their sensitivity to antibiotics
by a factor of 10(3)
Biofilm
• Neutrophilic granulocytes penetrate the biofilm
poorly and in the process lose their ability to
phagocytose.
• Apoptosis occurs with excessive complement
activation and release of radicals and proteases,
resulting in a local immune deficiency.
Biofilm
• In lower layers of the biofilm, conditions are
anaerobic, reducing growth rate and metabolic
activity of pathogens.
• Insensitive to antibiotics.
• After Tx has ended, return --->active mode, show
resistance to the originally administered AB
Biofilm
• return from sessile to planktonic phase is possible,
and clinically triggers local or systemic recurrence
of Ix.
• Biofilm population = permanent source of virulent
pathogens
• Safest Tx= surgical removal of sequestrum bearing
biofilm
Culprit bacteria
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Staph aureus,MRSA,epidermidis-65-70%
Gram –ve(biofilm forming pseudomonas)
Anaerobes
Polymicrobial-wound discharges
Others-gas gangrene
diagnosis
• A combination –clinical
-radiological
-pathological
n/b –biofilm shields the bacteria hence neg
bone /WBC scans
-bacteria at times in a semi dormant state – neg
cultures
clinical
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Pain
Loss of ROM
Swelling
Local warmth
Signs-sinus,effusion,wound erythema
investigations
• X rays-periosteal reaction,subchondral bone
resorption
• Aspiration
• Bone scan-Tc-not sensitive
-indium WBC –more sensitive
-others-marrow scans
-monoclonal ab scans
• Intraop frozen scans >5PMN/hpf –mirra
• Synovial biopsy-last resort
• pcr
classification
• GUSTILLO
• Early post op infection<4/52
• Late chronic>4/52
• Stage I
Coventry
within 3 months of surgery
o Usually transmitted at the time of surgery
o Staph and other gram positives most common
o Pain, wound drainage, erythema, induration
• Stage II
3-24 months
• Stage III >2 years post-surgery
o Usually caused by hematogenous spread to abnormal joint surfaces
o Joint pain predominates
Tsukayama and
colleagues-1996
1.+ve intraop cultures-iv antibiotics
2.Early post op infection -1/12
3.Late chronic infection
4.Acute haematogenous infection
musculoskeletal infection
society score
category
staging
description
Infection type
1
Early post op infection
<4/52
2
Haematogenous
infection<4/52
3
Late chronic infection
>4/52
A
UNCOMPROMISSED
B
Compromised <2
compromissing factor
C
Compromissed >2
compromissing factors
1
uncompromissed
2
Compromissed <2
Systemic host grade
Local extremity grade
Management
• Debridement with prosthesis retention
• Debridement with prosthesis removal
-one stage
-two stage
GOLD STANDARD
• 2 stage-removal of prosthesis
-I.V antibiotics 6/52
-cement spacer or prostalac
-use of cement in re implantation
-stemmed component
Salvaging failed re
implantation
• Options
1 fusion-those who may ambulate
2resection arthroplasty-fibrosis
3.amputation
Prognosis
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Poor if
Delayed diagnosis
Virulent organisms
Poor debridement
ISS
Host bed scarred and poor
• end