bone and joint infection Flashcards
—-Refers to inflammation of the bone or bone marrow
Usually caused by —-
can be — or —
- osteomyletis
- infection
- acute ( recent onset ) or chronic ( long term)
- mechanism of action :
1- — which is when organism for elsewhere spreads via —
as. vertebral osteomyelitis
/ discitis in an adult with
Staph. aureus endocarditis
2- — organism is directly into — and penetrates the injury , from adjacent focus of infection
- heamotegnous
- blood
- contagious
- heamotagenous osteomlytis :
1- in children its the emtaohysis of — affected , especially —- and —
2- in adults it affects –
- long bones
- tibia and femur
- vertebea
non homogenous om mechanism can be due to:
1- —- : penetrating injury/bites , contaminated open fractures
2- — : reconstruction of bones , prosthetic material as intra medullary nail , traumatic dental procedure
3- spread from adjacent —– focus as: acute from —– infection or chronic from —
- trauma
- surgery
- skin/soft tissue
- ear or sinus
- pressure sore or diabetic foot ulcers
causative pathogen in acute om:
- newborn less than 4:
- children from 4 months-4 years and metaphysics of long bones:
- children adolescent so more than 4 years
- adults ( mostly vertebrae) :
-S. aureus, group B Streptococcus, E. coli
-S. aureus, group A Streptococcus,
Streptococcus pneumoniae, Kingella kingae [Haemophilus influenzae (if not vaccinated),and Enterobacteriaceae]
-S. aureus (80%), group A Streptococcus
[H influenzae, and Enterobacteriaceae]
In sickle cell disease: non-typhoidal Salmonella
-S. aureus & occasionally Enterobacteriaceae or
Streptococcus spp.
Mycobacterium tuberculosis- endemic areas &
immunocompromised
Brucella spp. (uncommon in Ireland/ UK)
contagious om: pathogenesis:
1- it may be mono microbial or poly microbial
- — most common from eg.cellulitis/ soft tissue infection
- —- more common in children e.g. from ear or sinus infection
- cogualase — : after insertion of metal to stabilise a fracture
- polymicrobial w — : contaminated wound due to trauma, chronic
ulcers
- staph aurus most common
- streptococci ( Str. pneumoniae, group A strep)
- -ve staphlyococci
- gram -ve/anaerobes
chronic om: mechaism
1- usually due to — from —-
2- patient w poor — or multiple —
3- —–
3- —-
- Usually due to contiguous spread from pressure sore/
diabetic foot ulcer - Patients with poor mobility, multiple comorbidities
- Diabetes mellitus, peripheral vascular disease
- Non-acute presentation, usually present for some time at
diagnosis
chronic om pathogeen:
- Usually polymicrobial (> 1 organism), e.g. S. aureus
plus Gram negative bacilli plus anaerobes
– Organisms that colonise ulcers - Staphylococcus aureus (>50% cases)
- Anaerobes (10-20%) including Bacteroides/
Actinomyces - Gram negative bacilli, i.e. Pseudomonas
aeruginosa, E. coli, Klebsiella spp.
– Nosocomial infection
– Open wound/fracture
– May complicate trauma or surgery
– IV drug use
pathogenesis of om:
1- bacteria invade —
2- – within the bone increases due to —- ( 1,2 cause acute om)
3- fluid reaches — elevated it and bone —
4- separated periosteum produces —
5- — forms
- bone
- pressure
- inflammation and pus
- periosteum
- bone dies ( necrotic bone = sequestrum )
- new bone = involucre
- sinus tract
clinical features of om:
1- general :
2- local:
- general : ( which are seen in acute)
– fever
– malaise
– anorexia
– myalgia - local:
– pain
– tender
– hot
– swollen
( these above are more seen in acute)
– restricted motion
– pseudoparalysis
– fistula
– deformity
( last 2 are more seen in chronic )
acute vs chronic clinical features
1- acute:
- evolves over —
- no —
- fever , rigours , high acc
- In previously well patients
- If untreated for ≥10 days
(may be reflected by
ongoing clinical features),
get necrotic bone &
chronic osteomyelitis can
occur
2- chronic:
- evolves over:
- patient is —
- days/weeks
- necrosis/sinus tract
-Evolves over months/years
with low-grade
inflammation, dead bone
(sequestrum) & fistulous
tracts - Chronic pain
- Patient systemically well
- Usually co-morbidities
- Often relapses despite
apparently appropriate
treatment
Non-healing ulcer overlying bone or a chronically
discharging sinus, often a sign of underlying—-
chronic om
non microbiology diagnosis :
- History & examination
- Probe-to-bone test (chronic
osteomyelitis associated with
an ulcer) - Imaging:
– Plain X-ray, may be normal
– MRI, see bone oedema early
– Bone scan (nuclear) if MRI not
possible - Blood tests (non-specific)
– White cell count (elevated, neutrophilia)
– Inflammatory markers - ESR, CRP
- Histology on bone biopsy (in formalin)
– Pathological (not microbiological) diagnosis
microbiological diagnosis include:
- Biopsy of affected bone (not in formalin)
– Gram stain, culture & susceptibility testing
– Consider TB culture if chronic
– PCR: 16S ribosomal RNA - Pus/bone & not swab of ulcers/sinuses; may
grow colonising organisms & not deep
pathogens - Blood cultures if acute OM +/- systemic
symptoms, e.g. fever
– Diagnose if the patient is bacteraemic
in microbiological diagnosis:
* Identification of the — essential
to choose the best treatment
* —– is the gold
standard
* In suspected chronic OM, hold antibotics until – biopsy being taken
* A prospective study of bone biopsies showed a
sensitivity for OM of 87% & a specificity of 93%
- causative organism
- bone biopsy for culture and histology
- after
management of acute om :
* —- based on infecting organism
– Best response if started within 72h onset of symptoms
* Empiric treatment pending —- results must cover common causative organisms i.e. Staph. aureus
* Antibiotic treatment required for typically —-
– Usually IV for minimum 2-3 weeks followed by oral regimen
- intravenous antibiotics
- c+s
- 6 weeks
maangeming of acute om in specific treatment:
* If S. aureus:
– —- (MSSA) or —- (if MRSA)
* — may also be required if infected
fractures, delayed diagnosis
* Monitor response to treatment via clinical response/ESR + CRP (1-2 times/week)
- flucloxacillin
- vancomycin
- surgery
-in chronic om it cant be managed w —- alone
- same principle and treatment depends on — and —
- —- approach
- — debridement to remove necrotic bone if present and send for c+s
- treatment is more – minimum of 3/12 antibiotic therapy ]- success depends on extend of — of necrotic bone
- anitbitotc
- culture and suscpeitbitly results
- Multi-disciplinary team (MDT) as : pediatrist radiologist endocrinologist vascular surgeon diabetes nurse specialist tissue viability nurse ad microbiologist/ID physician
- surgical
- prolonged
- removal
prevention of om:
1- associated w surgery :
2- contiguous:
1-
* Peri-operative precautions to avoid
introducing bacteria into bone
* Appropriate pre-operative prophylaxis
2-
* Pressure sore prevention
* Diabetic foot care
—– Inflammation in the joint due to —
* Many other causes of arthritis that are not due to —
- septic arthritis
- infection
- infection
in septic arthritis:
1- invasion of — by micro organic usually w the extension into the joint space
2- any — agent may cause arthritis and — the most rapidly destructive
3- up to 25% loos of joint after infection is —-
4- pre-disposing factors include :
- synovial memebrane
- infectious
- bacteria
- irreversible
- Pre-existing joint disease
– RA: decreased polymorph
function, with reduced
chemotaxis
– OA - Prosthetic joints
- IVDU
- Diabetes mellitus
- Ulcerated skin
- Repeated intra-articular joint
injection
-septic arteries pathogenesis can be:
1- – organisms required to initiate a joint infection — > bacteria trigger an —- —> influx of —- –> release of – and – leads to — —> — subcentral bone loss can be seen within –
- hameotgenous and direct introduction
- few
- acute inflammatory synovitis
- acute and chronic inflammatory cells
- cytokines and proteases
- cartlige degradation
- irreversible
- days
clinical features include:
- Sudden onset of painful, hot swollen joint
- Joint swelling
– Knee > hip > shoulder > ankle/wrist
– Hip more common in children
– 10-20% polyarticular (2 or 3 joints) - More likely in patients with connective tissue disease
- Fever
- Source of infection elsewhere in 50%
– E.g. skin, lungs, bladder
causative organism :
1- — : 40-60% of cases
2- — : iv drug use
3- —: if penetrating trauma
age:
neonates —>
- children under 6 —>
- young children —>
- older adults —>
- staph. aureus
- Pseudomonas spp
- aerobes
- E. coli, Grp B streptococcus (bloodstream infecection)
-children under 6:
Staph. aureus,
Strep. pneumoniae,
Strep. pyogenes (group A strep)
Kingella kingae - young aults: N. gonorrhoeae, Staph. aureus
- older adults:
Staph. aureus,
Strep. pneumoniae,
Strep. pyogenes,
Gram negative bacilli (e.g., E. coli)
Staph. epidermidis– if prosthesis
gonococcal septic arthritis :
- septic — or — arthritis
- may occur in association w other disseminated gonococcal infection :
- mono or oligo
– Migratory polyarthritis
– Tenosynovitis: wrist, ankles & small
joints
– Skin lesions: multiple painless
macules, papules arms, legs, trunk
– Fever
diagnosis - microbiology
- Joint aspiration to obtain synovial fluid (pre-antibiotics)
- Microscopy – white cell count (high, predominantly neutrophils)
– Gram stain (ZN stain) -up to 50% of microscopy positive (25% in
gonococcal)
– Microscopy for crystals to rule out gout etc. - Culture– up to 90% culture positive
– 50% in gonococcal - PCR
– Pathogen specific – e.g. gonococcal
– Pan-bacterial e.g. 16S ribosomal RNA - Blood culture, almost 50% positive
- Urine / genital swabs (if ? gonococcal)
- Serology only if indicated:
– Anti-Streptolysin O Titre (ASOT)
– Brucella
– Syphilis (rare)
– Leptospira (rare)
– Borrelia burgdorferi (Lyme disease)
diagnosis - non microbiology :
- Bloods (non-specific)
– WCC, ESR, CRP
– Urea and electrolytes, LFTs - Diagnostic imaging
– Plain X-ray - Not diagnostic but baseline for assessing future joint
damage - May see effusion
– MRI – can’t distinguish infection vs. inflammation
early on
– May require ultrasound to get fluid specimen
treatment:
- Surgical drainage - remove pus
– Aspiration
– Arthroscopic washout
– Suction drain - IV antibiotics
– For > 2 wks, then oral for another 2-4 wks
– Optimum duration unknown
– e.g. flucloxacillin empirically for native joint pending
culture & susceptibility
– Gonococcal arthritis - ceftriaxone - Monitor inflammatory markers (CRP)
tuberceuloriss of bone and joints :
- pathogen :
- increased incidence due to —
- found in:
- clinical features include:
- mycobacterium tuberculosis
- hIV
- spine T10/11 ( which can cause Potts disease) , hip , knee for weight bearing
- includes:
- Slow onset of chronic monoarthritis
- Usually no systemic symptoms
- Swelling may be marked, but signs of acute inflammation
absent or mild - Spinal TB
– Collapse of intravertebral disc
– Psoas abscess – may spread to groin
– Paraplegia secondary to pressure on spinal cord
- tuberculosis of bone n joints :
1- diagnosis:
2- management
1-
* Aspirate
* TB PCR
* ZN / Auramine stain
* Culture
– Synovial fluid culture
positive in 80-90%
* Imaging: see joint
space narrowing &
bone erosions
2-
* Anti-TB drugs usually
eradicate, but may
need surgery
* Prolonged treatment
required for up to 12
months
Septic arthritis or OM involving a —- which is total hip replacement and diganosis is complex
managed by :
- prosthetic joint
- – Surgical drainage/debridement/removal of implant
– Antimicrobial therapy – usually prolonged (weeks to
months)
